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Stems are a part of the shoot system of a plant. It also helps to transport the products of photosynthesis, namely sugars, from the leaves to the rest of the plant.
Plant stems, whether above or below ground, are characterized by the presence of nodes and internodes (Figure 1). Nodes are points of attachment for leaves, aerial roots, and flowers. The stem region between two nodes is called an internode. The stalk that extends from the stem to the base of the leaf is the petiole. An axillary bud is usually found in the axil—the area between the base of a leaf and the stem—where it can give rise to a branch or a flower. The apex (tip) of the shoot contains the apical meristem within the apical bud.
The stem and other plant organs arise from the ground tissue, and are primarily made up of simple tissues formed from three types of cells: parenchyma, collenchyma, and sclerenchyma cells.
Parenchyma cells are the most common plant cells (Figure 2). They are found in the stem, the root, the inside of the leaf, and the pulp of the fruit. Parenchyma cells are responsible for metabolic functions, such as photosynthesis, and they help repair and heal wounds. Some parenchyma cells also store starch. In Figure 2, we see the central pith (greenish-blue, in the center) and peripheral cortex (narrow zone 3–5 cells thick just inside the epidermis); both are composed of parenchyma cells. Vascular tissue composed of xylem (red) and phloem tissue (green, between the xylem and cortex) surrounds the pith.
Collenchyma cells are elongated cells with unevenly thickened walls (Figure 3). They provide structural support, mainly to the stem and leaves. These cells are alive at maturity and are usually found below the epidermis. The “strings” of a celery stalk are an example of collenchyma cells.
Sclerenchyma cells also provide support to the plant, but unlike collenchyma cells, many of them are dead at maturity. There are two types of sclerenchyma cells: fibers and sclereids. Both types have secondary cell walls that are thickened with deposits of lignin, an organic compound that is a key component of wood. Fibers are long, slender cells; sclereids are smaller-sized. Sclereids give pears their gritty texture. Humans use sclerenchyma fibers to make linen and rope (Figure 4).
Which layers of the stem are made of parenchyma cells?
- cortex and pith
[reveal-answer q=”700313″]Show Answer[/reveal-answer]
[hidden-answer a=”700313″]Answer a and b. The cortex, pith, and epidermis are made of parenchyma cells.[/hidden-answer]
Some plant species have modified stems that are especially suited to a particular habitat and environment (Figure 5). A rhizome is a modified stem that grows horizontally underground and has nodes and internodes. Vertical shoots may arise from the buds on the rhizome of some plants, such as ginger and ferns. Corms are similar to rhizomes, except they are more rounded and fleshy (such as in gladiolus). Corms contain stored food that enables some plants to survive the winter. Stolons are stems that run almost parallel to the ground, or just below the surface, and can give rise to new plants at the nodes. Runners are a type of stolon that runs above the ground and produces new clone plants at nodes at varying intervals: strawberries are an example. Tubers are modified stems that may store starch, as seen in the potato (Solanum sp.). Tubers arise as swollen ends of stolons, and contain many adventitious or unusual buds (familiar to us as the “eyes” on potatoes). A bulb, which functions as an underground storage unit, is a modification of a stem that has the appearance of enlarged fleshy leaves emerging from the stem or surrounding the base of the stem, as seen in the iris.
Watch botanist Wendy Hodgson, of Desert Botanical Garden in Phoenix, Arizona, explain how agave plants were cultivated for food hundreds of years ago in the Arizona desert in this video: Finding the Roots of an Ancient Crop.
A link to an interactive elements can be found at the bottom of this page.
Some aerial modifications of stems are tendrils and thorns (Figure 6). Tendrils are slender, twining strands that enable a plant (like a vine or pumpkin) to seek support by climbing on other surfaces. Thorns are modified branches appearing as sharp outgrowths that protect the plant; common examples include roses, Osage orange and devil’s walking stick.
2016 STEM Summer Camp on DNA Biology and Bioinformatics
In the first part of Thursday's lesson, the students used dissection microscopes to examine bees as they learned about their anatomy and biology.
The second part seemed like it involved a completely different field: In it, students learned about programming basics.
But this particular camp for high school students at Oregon State University was focused on DNA and bioinformatics, a field that specializes in using data tools to aid scientists, so the skill was actually an intrinsic part of the field. The camp, which ends today, is one of 30 summer camps put on by OSU’s Science, Technology, Engineering and Math Academy, part of the university's precollege program.
Cathy Law, the head of the STEM Academy, said the camps, which are mostly day camps, served more than 500 students last summer and attract students from across the state. They even attract a handful of students from outside the country.
She said the purpose of the camps is not just to highlight STEM fields and OSU, but also to offer general encouragement to students to pursue education beyond high school, even if that is community college.
The program gave out $11,000 in scholarships last year for the camps, Law said.
Pankaj Jaiswal, an associate professor in the department of plant pathology who organized the DNA and bioinformatics camp, said that students in the camp got to do hands-on science activities that many graduate students in the field haven’t done.
Jaiswal said he’s organized the camp since the summer of 2013 as a way to engage students in science early and potentially bring them into the field. It also helps him meet outreach requirements in his National Science Foundation grants.
In addition to the bee activity, students tackled bacterial genome sequencing, stained and visualized skin tumor samples they also processed, and cultured malignant cancer cells and did cancer cell imaging, analysis, and phenotyping.
Jaiswal said the common theme through the lessons: they're all connected to DNA, the genome, and genetics.
He said organizers structure the camp to emphasize hands-on activities rather than just listening to lectures. Doing activities by hand, he said, "is a different experience as it helps in retaining the knowledge."
Kirah Lucier, a White City resident who will start her sophomore year at Eagle Point High School this fall, said she decided to do the camp because she likes science.
“Science is one of the few things I’ve had in school that really spikes my interest,” she said. And the hands-on activities are central to that.
“For me, a hands-on experience helps me learn better,” she said. “With hands-on activities you get experience and you get to have fun.”
Human embryonic stem cells carrying an unbalanced translocation demonstrate impaired differentiation into trophoblasts: an in vitro model of human implantation failure
Carriers of the balanced translocation t(1122), the most common reciprocal translocation in humans, are at high risk of creating gametes with unbalanced translocation, leading to repeated miscarriages. Current research models for studying translocated embryos and the biological basis for their implantation failure are limited. The aim of this study was to elucidate whether human embryonic stem cells (hESCs) carrying the unbalanced chromosomal translocation t(1122) can provide an explanation for repeated miscarriages of unbalanced translocated embryos. Fluorescent in situ hybridization and karyotype analysis were performed to analyze the t(1122) in embryos during PGD and in the derived hESC line. The hESC line was characterized by RT-PCR and FACS analysis for pluripotent markers. Directed differentiation to trophoblasts was carried out by bone morphogenetic protein 4 (BMP4). Trophoblast development was analyzed by measuring β-hCG secretion, by β-hCG immunostaining and by gene expression of trophoblastic markers. We derived the first hESC line carrying unbalanced t(1122), which showed the typical morphological and molecular characteristics of a hESC line. Control hESCs differentiated into trophoblasts secreted increasing levels of β-hCG and concomitantly expressed the trophoblast genes, CDX2, TP63, KRT7, ERVW1, CGA, GCM1, KLF4 and PPARG. In contrast, differentiated translocated hESCs displayed reduced and delayed secretion of β-hCG concomitant with impaired expression of the trophoblastic genes. The reduced activation of trophoblastic genes may be responsible for the impaired trophoblastic differentiation in t(1122)-hESCs, associated with implantation failure in unbalanced t(1122) embryos. Our t(1122) hESCs are presented as a valuable human model for studying the mechanisms underlying implantation failure.
Keywords: human embryonic stem cells implantation failure preimplantation genetic diagnosis trophoblast differentiation unbalanced translocation.
A Path From Questions to Answers to Solutions
If the stem cell wars are indeed over, no one will savor the peace more than James Thomson.
Dr. Thomson’s lab at the University of Wisconsin was one of two that in 1998 plucked stem cells from human embryos for the first time, destroying the embryos in the process and touching off a divisive national debate.
And on Tuesday, his lab was one of two that reported a new way to turn ordinary human skin cells into what appear to be embryonic stem cells without ever using a human embryo.
The fact is, Dr. Thomson said in an interview, he had ethical concerns about embryonic research from the outset, even though he knew such research offered insights into human development and the potential for powerful new treatments for disease.
“If human embryonic stem cell research does not make you at least a little bit uncomfortable, you have not thought about it enough,” he said. “I thought long and hard about whether I would do it.”
He decided in the end to go ahead, reasoning that the work was important and that he was using embryos from fertility clinics that would have been destroyed otherwise. The couples whose sperm and eggs were used to create the embryos had said they no longer wanted them. Nonetheless, Dr. Thomson said, announcing that he had obtained human embryonic stem cells was “scary,” adding, “it was not known how it would be received.”
But he never anticipated the extent and rancor of the stem cell debate. For nearly a decade now, the issue has bitterly divided patients and politicians, religious groups and researchers.
Now with the new technique, which involves just adding four genes to ordinary adult skin cells, it will not be long, he says, before the stem cell wars are a distant memory. “A decade from now, this will be just a funny historical footnote,” he said in the interview.
As for the science behind it, the thrill of discovery, he said there was never a “eureka.”
“Surprisingly, there is no ‘Wow’ moment,” he said, either from 1998 or now. Both times, the discovery came after he’d spent months rigorously testing the cells to be sure they really were stem cells, worrying all the while that they could die or be lost to contamination. When he knew he had succeeded, the suspense was gone.
“Imagine holding your breath for a few months,” Dr. Thomson said. When he was done, he said, “I felt mostly a sense of relief.”
But he knows what he wrought. Stem cells, universal cells that can turn into any of the body’s 220 cell types, from brain to lung, from liver to heart to skin, normally emerge only fleetingly after a few days of embryo development. Scientists want to use them to study complex human diseases like Alzheimer’s or Parkinson’s in a Petri dish, finding causes and treatments. And, they say, it may be possible to use the cells to grow replacement tissues for patients.
The problem until now had been the source of the cells — human embryos.
The topic, says R. Alta Charo, a University of Wisconsin ethicist, “took on an almost iconic quality the same way Roe versus Wade has.”
In the meantime, many leading scientists decided not to get into the stem cell field. There was a stigma attached, Dr. Thomson says. And, he adds, “most scientists don’t like controversial things.”
A native of Oak Park, Ill., James Alexander Thomson, now 48, did not set out to throw bioethical bombs. All he wanted, he said, was to answer the most basic scientific questions about cellular development.
First there was a degree in biophysics from the University of Illinois. As a graduate student, Dr. Thomson began working with mouse embryonic stem cells and then, with federal support, he extracted stem cells from monkey embryos. After earning two doctorates from the University of Pennsylvania, one in veterinary medicine and one in molecular biology, he continued research at his own lab at the University of Wisconsin. Eventually he realized, though, that studying mice and monkeys could only take him so far. If he wanted to understand how human embryos develop and why their development sometimes goes awry, he needed human stem cells. But, he says, he hesitated.
In 1995, he began consulting with two ethicists at his university, Dr. Norman Fost, a physician, and Ms. Charo, a law professor. His plan was to use unwanted embryos from a fertility clinic.
“It is unusual in the history of science for a scientist to really want to think carefully about the ethical implications of his work before he sets out to do it,” Dr. Fost said. “The biggest problem in ethics is not anticipating problems.”
But Dr. Fost and Dr. Thomson guessed wrong about what would bother people most. They thought it would be what Dr. Fost termed “the technological power” of stem cells. What if someone put human stem cells into the brain of a rat, for example?
“I thought at the time that this was possibly the biggest issue,” Dr. Fost said. “It was unprecedented in the history of biology. It’s the ‘Help. Get me out of here’ scenario. Let’s say the rat brain turns out to be entirely human cells. What’s going on in there? Is it a human brain? And how would you study it? You can’t ask the rat.”
Meanwhile, as Dr. Thomson was planning his attempt to obtain human embryonic stem cells, another discovery changed his entire view of development. In 1997, Ian Wilmut, a scientist in Scotland, announced that the creation of the first cloned mammal, Dolly, cloned from frozen udder cells from a long-dead sheep.
Dr. Wilmut had slipped an udder cell — a cell that normally would never be anything but an udder cell — into an egg whose genetic material had been removed. The egg somehow brought the udder cell’s chromosomes back to the state they had been in when embryo development first began.
“Dolly changed the way I thought about developmental biology,” Dr. Thomson says. “Development was reversible.”
Four years ago he and, independently, Shinya Yamanaka of Kyoto University, set out to figure out a way to mimic what an egg can do. Both groups succeeded and both discovered that all they had to do was add four genes to the cells and the cells would turn into cells that look, so far, just like stem cells.
“It is actually fairly straightforward to repeat what we have done,” Dr. Thomson said. More work remains, but he is confident that the path ahead is clear.
Entering the era of single-cell transcriptomics in biology and medicine
Recent technical advances have enabled RNA sequencing (RNA-seq) in single cells. Exploratory studies have already led to insights into the dynamics of differentiation, cellular responses to stimulation and the stochastic nature of transcription. We are entering an era of single-cell transcriptomics that holds promise to substantially impact biology and medicine.
Our notion of transcriptomes has been forged mainly by population-level observations that have been the mainstream in biology over the last two decades. We are used to thinking about differences in expression in terms of graded or subtle fold changes when comparing data across entire tissues or conditions. But the actual differences between cells may be far larger. Subsets of cells may experience dramatic changes that are averaged out or diluted by the presence of a large number of nonresponsive cells. In fact, it was shown over 60 years ago that inductive cues often result in all-or-none responses in single cells but these responses are observed as a gradual increase when quantified across the population 1 .
Part 2: Making the Right Choice
00:00:15.06 Welcome back, everyone.
00:00:16.22 So, again, I'm Jeanie Lee.
00:00:18.18 I'm a Professor of Genetics at Harvard Medical School,
00:00:21.21 and I'm also a faculty member in the Department of Molecular Biology
00:00:24.17 at Massachusetts General Hospital.
00:00:27.00 Now, in Lecture 1,
00:00:28.22 I gave an overview of X chromosome inactivation.
00:00:31.23 And what we're gonna do now in Lecture 2
00:00:33.27 is a deeper dive into the initiation phase of inactivation,
00:00:38.27 namely how cells count
00:00:41.15 and then make the correct choice
00:00:43.29 of active and inactive chromosomes.
00:00:46.22 So, here again are the different steps of X inactivation.
00:00:49.20 And by way of review, there's a counting mechanism followed by a choice mechanism,
00:00:53.27 and then the initiation of silencing.
00:00:57.28 So, we're gonna focus first on the counting step.
00:01:01.25 So, again, this takes place in the blastocyst,
00:01:04.25 shortly after the paternal X chromosome is reactivated.
00:01:08.07 And every cell makes its own determination
00:01:11.14 of the X chromosome number.
00:01:13.14 So, it's taking place around the time
00:01:15.15 that the epiblast has 20 cells or so.
00:01:20.29 And we discussed how it's really the X-to-autosome ratio
00:01:24.09 that cells are sensing,
00:01:25.23 rather than the absolute number of X chromosomes.
00:01:27.27 And we also mentioned that cells
00:01:31.05 follow the n-1 rule per diploid content,
00:01:34.00 so that males who have an X-to-autosome ratio of 0.5
00:01:39.02 will not inactivate any chromosomes,
00:01:42.04 regardless of whether it's diploid or tetraploid,
00:01:45.22 with twice the genomic content.
00:01:47.26 Whereas the female,
00:01:49.28 with an X-to-autosome ratio of 1.0,
00:01:52.10 will inactivate one of her two X chromosomes,
00:01:55.24 and if she's tetraploid she'll inactivate
00:01:58.11 two out of those four X chromosomes.
00:02:00.23 And furthermore, if the diploid had three X chromosomes,
00:02:04.10 it will inactivate two out of the three.
00:02:07.10 And if she has four X chromosomes,
00:02:10.21 she'll inactivate three out four.
00:02:12.27 And so the point is that cells follow this n-1 rule
00:02:16.06 in a diploid content,
00:02:17.26 and every cell makes the determination for itself.
00:02:21.07 And we also mentioned that
00:02:24.20 counting is most likely a titration of X-linked
00:02:27.08 and autosomal factors.
00:02:28.25 We mentioned that the numerators
00:02:30.21 are produced from the X chromosome,
00:02:33.22 in the form of this green blob.
00:02:35.26 And the autosomes also produce their own factors
00:02:39.17 -- we call them denominators.
00:02:41.12 And then the red and green factors
00:02:43.15 will titrate each other out,
00:02:45.04 and form a blocking factor
00:02:47.03 that then sits on one X chromosome,
00:02:50.08 at the inactivation center,
00:02:51.20 and prevents that inactivation center
00:02:54.19 from initiating the cascade of inactivation.
00:02:58.03 So, we see that in the male cell.
00:03:00.15 And we also see that in the female cell,
00:03:02.20 where the same factors titrate each other out
00:03:06.11 to form a hypothetical blocking factor,
00:03:08.26 which then sits on the.
00:03:11.25 one X chromosome, preventing that inactivation center from firing,
00:03:15.11 giving rise to this privileged, active X chromosome.
00:03:19.27 And we mentioned that one hypothesis
00:03:22.21 is that the remaining X chromosomes
00:03:25.11 would then undergo an inactivation by default.
00:03:28.22 So, that's certainly one viable viewpoint.
00:03:31.10 However, we favor the idea that there is a purposeful inactivation
00:03:35.17 -- not something that happens by default.
00:03:37.17 Because, in fact, the female produces
00:03:40.29 an extra copy of these green factors,
00:03:44.12 since she has one extra X chromosome.
00:03:46.21 And that green factor is not titrated by the blocking factor,
00:03:50.18 so we propose that that factor
00:03:53.25 goes and forms this additional complex
00:03:58.01 called a competence factor,
00:04:00.08 which has to sit on the remaining X chromosome
00:04:04.00 to purposely induce the initiation of inactivation.
00:04:08.22 So, that's the two factors hypothesis.
00:04:13.12 So, then we get down to,
00:04:15.14 what are these molecular factors
00:04:18.29 that make up the X, right?
00:04:21.02 And what are the factors that make up
00:04:22.29 the A of the X-to-autosome ratio?
00:04:25.09 And here we'll start with the numerator, the X.
00:04:29.04 So, in principle, without knowing all that much
00:04:31.16 about what these factors are,
00:04:33.08 we can say that the factor
00:04:35.22 has to be produced from the X inactivation center
00:04:37.25 -- from those transgenesis experiments that I showed you before.
00:04:40.21 And we believe that that factor
00:04:43.20 has to escape X inactivation.
00:04:46.02 So, I haven't mentioned before,
00:04:47.26 but a number of genes on this chromosome
00:04:51.04 are actually immune to the influence of Xist.
00:04:55.26 They escape silencing.
00:04:57.17 And we believe that numerators
00:04:59.22 have to escape X inactivation
00:05:02.01 in order to serve as a dosage-sensitive readout
00:05:05.29 of that chromosome.
00:05:08.17 And furthermore, that factor has to be diffusible.
00:05:11.16 So, in order to titrate away autosomal factors,
00:05:13.17 it has to be able to move around in the nucleus.
00:05:16.24 And then finally,
00:05:18.18 it has to act at the X inactivation center,
00:05:20.25 which is where the Xist gene ultimately resides.
00:05:24.23 And then, most importantly,
00:05:26.20 the math has to work.
00:05:28.10 And what I mean by that is,
00:05:30.14 if something were truly a numerator,
00:05:33.13 then when we take away one copy of that X-linked numerator,
00:05:38.16 a female's cells should start to behave like male cells
00:05:42.22 and block X inactivation.
00:05:46.09 So, she should think that she's a male cell,
00:05:48.01 because she's missing the extra X-linked factor.
00:05:50.27 And conversely,
00:05:53.14 if we were to give a male cell extra copies of a numerator,
00:05:57.05 that male cell has to start to behave like a female cell
00:06:00.14 and start undergoing X chromosome inactivation.
00:06:05.19 So, these are the rules.
00:06:07.08 Now, a while back,
00:06:09.10 we started to suspect this non-coding gene, Jpx,
00:06:12.21 which lies just on the other side of Xist.
00:06:15.23 It's an X-linked Xic product.
00:06:18.16 We know that Jpx levels
00:06:21.27 increase about tenfold during the process of X inactivation.
00:06:24.29 And it occurs in the same timeframe that Xist
00:06:29.01 is getting upregulated on that chromosome,
00:06:31.15 and we know that it escapes X inactivation.
00:06:33.29 It's one of the few genes that will escape inactivation.
00:06:36.27 And from the transgenesis experiments.
00:06:39.26 I told you before, when we move this region
00:06:41.27 and put it on an autosome,
00:06:43.14 that autosome behaves like an X chromosome
00:06:45.18 and undergoes inactivation.
00:06:47.09 However, if we were to make a transgene
00:06:50.04 that's missing this Jpx,
00:06:53.14 that transgene could no longer inactivate the autosome.
00:06:59.29 So, we put this to the test.
00:07:03.16 So, here. this is an RNA fluorescence in situ experiment,
00:07:06.23 in which we're looking at expression of Xist,
00:07:09.06 which is shown here as a pink dot,
00:07:12.00 and it's coating the X chromosome.
00:07:14.16 So, in wildtype cells we see a very robust expression of Xist RNA.
00:07:19.15 Now, if we, in the female cell,
00:07:21.29 deleted just one copy of Jpx.
00:07:25.07 so, there are two copies normally.
00:07:27.06 we just take away one copy of Jpx.
00:07:29.00 you see that these cells no longer produce that
00:07:32.14 large, robust cloud of RNA
00:07:35.20 that coats the inactive X chromosome.
00:07:38.05 However, if we then take a copy of Jpx
00:07:41.16 and insert it into another chromosome, an autosome,
00:07:46.03 we rescue this expression of Xist
00:07:50.15 in the same female cells.
00:07:53.22 So, these experiments tell us two very important things.
00:07:56.13 First of all, Jpx is a dosage-sensitive element.
00:08:01.18 So, by removing one copy of Jpx
00:08:04.25 in these female cells,
00:08:06.17 the female cells start to behave like a male cell.
00:08:09.26 And furthermore, Jpx is diffusible,
00:08:13.19 because we put the gene on an autosome.
00:08:16.02 That autosomally produced Jpx will rescue Xist expression
00:08:20.18 on the X chromosome.
00:08:22.17 And then we did the converse experiment,
00:08:24.27 where, in male cells now,
00:08:27.06 we insert extra copies of Jpx.
00:08:30.04 Male cells normally don't produce Xist at all,
00:08:32.13 so you don't see a big Xist spot in green.
00:08:35.04 But when we insert extra copies of Jpx
00:08:38.22 into these male cells,
00:08:40.16 you start to see Xist expression go up, okay?
00:08:45.03 So, that suggests that Jpx may in fact
00:08:48.00 be a candidate for a numerator factor.
00:08:51.15 And in this experiment, here,
00:08:53.29 we're demonstrating that Jpx is acting as a diffusible RNA,
00:08:58.07 one of these long non-coding RNAs.
00:09:00.06 And it's not simply the genetic element, the DNA,
00:09:04.04 which is responsible for this counting act.
00:09:06.18 And we know that because
00:09:09.26 when we introduce these things called shRNAs.
00:09:12.11 this is a technology that allows us to degrade the RNA
00:09:15.17 when we introduce the shRNA into cells,
00:09:18.07 without actually touching the underlying gene.
00:09:22.00 Okay, so when we introduce these RNA degradation factors,
00:09:25.15 we see that Xist could no longer be upregulated,
00:09:29.25 like in the wildtype female cell,
00:09:32.06 or the untouched female cell.
00:09:34.15 So, this experiment tells us that
00:09:38.02 Jpx is a diffusible element, acting as a non-coding RNA.
00:09:44.24 So, the idea then is that
00:09:47.09 Jpx is one of these green factors
00:09:49.26 that's being produced by the X chromosome,
00:09:51.25 and that it is titrating away the autosomal blocking factor.
00:09:56.09 And then the untitrated Jpx factors
00:09:59.22 would be the one that sits on the remaining inactive X
00:10:04.19 to induce the firing of that inactivation center.
00:10:09.00 So then, we turn our attention to,
00:10:10.29 what are the pink factors?
00:10:12.15 What are these autosomal factors
00:10:14.15 which are getting expressed to titrate Jpx?
00:10:18.19 Now, here, we began to suspect
00:10:21.03 a protein called CTCF.
00:10:23.19 Now, CTCF is a very famous protein
00:10:26.01 because it does a lot of different things.
00:10:28.02 It has been shown to be a critical chromosome architectural factor.
00:10:32.15 It was first identified by Victor Lobanenkov
00:10:34.23 as an 11-zinc finger transcription factor
00:10:38.01 that can take two distant genetic elements
00:10:41.26 and bring them together to form a loop,
00:10:44.08 as shown here,
00:10:45.23 and can regulate enhancer-promoter interactions.
00:10:50.03 And more recently, CTCF has been shown to
00:10:53.20 reside at the border of these chromosomal topological structures
00:10:56.17 called TADs,
00:10:58.00 and I'll say a lot more about that in lecture number 3.
00:11:03.07 But importantly, we've known for quite some time that
00:11:05.25 CTCF occupies discrete positions
00:11:08.29 at the X inactivation center
00:11:11.11 and plays an important role in a number of different processes.
00:11:15.16 So, for example, here
00:11:18.29 CTCF binds to the Xist promoter at a number of positions
00:11:21.23 that are shown here in red.
00:11:23.25 And we know that at these sites
00:11:26.07 CTCF is serving as a repressor of the Xist gene.
00:11:31.01 And then, as cells go through X inactivation,
00:11:33.12 these binding sites here
00:11:35.16 -- shown, again, in red --
00:11:37.14 pretty much stay the same.
00:11:39.20 They remain bound.
00:11:41.17 Except for one. at one location,
00:11:43.23 the so-called P2 location.
00:11:45.29 Now, at this position,
00:11:48.17 CTCF binding actually goes down during X inactivation.
00:11:53.25 So, that was really interesting.
00:11:55.17 And we wanted to know,
00:11:57.07 because there are two X chromosomes,
00:11:58.24 from which X chromosome CTCF was getting removed.
00:12:01.22 So, for that, we had to perform
00:12:04.02 an allele-specific analysis.
00:12:05.29 You know. so, that's an analysis that allows us to
00:12:08.10 tell the difference between the future active
00:12:10.11 and the future inactive chromosomes.
00:12:12.17 And the long and the short of this is that it is from the future inactive.
00:12:17.19 the chromosome which will become inactivated.
00:12:19.22 that's where CTCF is losing its binding.
00:12:24.08 Okay. So, during X inactivation,
00:12:28.08 CTCF at P2 is retained only on the active X chromosome.
00:12:31.26 And we know that its role is to
00:12:34.24 block the expression of this critical silencing factor called Xist.
00:12:39.14 So, what I've told you, then,
00:12:41.13 is that CTCF is an autosomal factor.
00:12:45.14 It represses Xist expression.
00:12:48.00 And at the same time,
00:12:49.25 I've told you that this non-coding RNA that's X-linked
00:12:54.12 induces Xist expression.
00:12:56.26 And so, with one being autosomal,
00:12:58.25 the other one being X-linked,
00:13:00.16 and doing opposite things,
00:13:02.19 we wondered whether these two factors
00:13:05.13 could be functionally interacting with each other,
00:13:07.16 and be part of that titration mechanism
00:13:10.04 that I referred to earlier,
00:13:12.07 part of the X inactiv. the X-to-autosome ratio.
00:13:16.03 So, indeed, we learned that CTCF is an RNA-binding protein.
00:13:22.01 That was not previously known to bind RNA.
00:13:24.25 But in this context,
00:13:26.25 it is a very good RNA-binding protein.
00:13:28.20 In fact, it prefers to bind RNA over DNA.
00:13:31.22 So, you can see from the same sort of gel shift analysis, here.
00:13:35.03 except that this time we're using Jpx RNA,
00:13:38.15 and you see that very robust shift,
00:13:40.10 indicating a high-affinity binding
00:13:43.04 between the RNA and CTCF protein.
00:13:45.20 And so, in fact, we can biochemically
00:13:48.26 measure the affinity of this complex
00:13:51.05 by measuring the dissociation constant.
00:13:54.16 And that Kd is less than one nanomolar.
00:13:57.14 So, CTCF is a very good RNA binding protein,
00:14:00.20 much better than binding to.
00:14:03.15 its binding to DNA,
00:14:05.26 where the dissociation constant is more than 20 nanomolar.
00:14:14.21 So, then we have this idea that
00:14:17.13 CTCF may be getting competed away from the promoter
00:14:20.10 by this non-coding RNA, Jpx,
00:14:24.01 and that may underlie this titration mechanism.
00:14:27.06 And so to test that,
00:14:29.10 we mixed together purified components of P2 DNA,
00:14:34.00 CTCF bound to the P2 DNA,
00:14:37.12 and increasing concentrations of this Jpx RNA.
00:14:41.08 And what we see here in this gel shift analysis
00:14:44.28 is that CTCF gets pulled away from the DNA
00:14:49.10 by Jpx RNA.
00:14:53.22 So, we can do the same sort of competition experiment
00:14:56.17 inside of cells.
00:14:58.12 Now, what I've shown you so far
00:15:00.23 occurred within a test tube, right?,
00:15:02.17 but we can do this sort of thing inside a cell as well.
00:15:05.23 So, here, we're overexpressing CTCF
00:15:09.10 -- that's the repressor of Xist --
00:15:11.03 and you can see that when we do that
00:15:13.20 the cells no longer upregulate this green cloud of Xist.
00:15:17.08 So, here's wildtype, as you can see.
00:15:19.20 But in the overexpression system,
00:15:22.12 we no longer see Xist clouds.
00:15:26.00 However, we can overcome these extra quantities,
00:15:31.08 if you will,
00:15:33.14 of CTCF by giving the cells extra Jpx RNA.
00:15:37.23 And so that's what we've done here.
00:15:39.05 And you see that these green spots come back.
00:15:44.01 So, that supports this idea that
00:15:47.22 CTCF and Jpx RNA are functionally interacting with each other
00:15:51.16 and titrating each other inside of cells.
00:15:55.22 So, what we propose, then,
00:15:58.26 is a functional antagonism between CTCF and Jpx RNA.
00:16:03.04 So, prior to X inactivation,
00:16:05.04 CTCF sits very robustly at the 5' end of Xist,
00:16:08.24 where it blocks the expression of Xist.
00:16:11.24 And then, at the onset of X inactivation,
00:16:15.09 what we have empirically measured is that Jpx RNA
00:16:19.28 increases in expression by tenfold.
00:16:22.10 And when it crosses a certain threshold,
00:16:25.05 as it will do only in female cells
00:16:27.03 -- because we have twice the number of Jpx copies as male cells --
00:16:32.07 the Jpx RNA binds to CTCF
00:16:36.03 and titrates it away from one Xist promoter.
00:16:40.21 And that act enables Xist RNA
00:16:44.14 to be upregulated on that same chromosome.
00:16:49.06 So, that's how we're presently thinking about
00:16:52.00 this functional antagonism
00:16:54.08 and about the X-to-autosome ratio.
00:16:57.04 What I'd now like to turn your attention to
00:16:59.23 is the second step of X inactivation,
00:17:02.00 which is allelic choice.
00:17:04.05 And I mentioned in the first lecture
00:17:06.18 that this is a conceptually very challenging problem,
00:17:09.01 because, here, choice has to be random.
00:17:14.10 It has to be instantaneous,
00:17:17.17 mutually exclusive,
00:17:19.04 and completely irreversible.
00:17:23.03 So, how do we make the right choice.
00:17:24.22 And again, we believe that there is a communication
00:17:27.19 between the two chromosomes,
00:17:29.01 such that when one chromosome is chosen as the inactive one
00:17:31.19 the other one is instantaneously the active chromosome.
00:17:36.28 So, this mutually exclusive choice
00:17:39.14 -- which is what we call it --
00:17:40.28 requires two genetic loci at the X inactivation center.
00:17:44.25 So, one is Xist's antisense repressor,
00:17:49.23 called Tsix, shown here in yellow,
00:17:52.11 and the other its enhancer,
00:17:54.21 shown here in brown, called Xite.
00:17:59.12 So, the region that's responsible for choice
00:18:01.09 is this 15 kilobase domain
00:18:03.21 that encompasses Tsix and Xite.
00:18:06.13 And what we know
00:18:08.23 -- going back to experiments done many, many years ago --
00:18:11.08 is that prior to X inactivation,
00:18:13.22 when the two chromosomes are active,
00:18:15.25 the Tsix antisense RNA is expressed at very high levels,
00:18:20.22 and its expression prevents Xist from turning up.
00:18:27.27 But then, at the onset of X inactivation,
00:18:30.01 what happens is that
00:18:32.27 the antisense RNA disappears from one X chromosome.
00:18:36.07 And when it disappears,
00:18:38.05 Xist RNA is upregulated from that chromosome,
00:18:41.18 leading to the formation of the inactive X.
00:18:44.23 While on the other X chromosome,
00:18:47.07 the action of the Xite enhancer, right?,
00:18:52.29 allows Tsix to persist on that chromosome,
00:18:58.04 so that the Xist gene continues to be repressed
00:19:01.12 on that chromosome.
00:19:03.13 And that chromosome stays active.
00:19:05.18 So, the action of Tsix is essential for this mutually.
00:19:09.22 for this allelic choice, with its persistence on the active.
00:19:15.09 its persistence determining the active X chromosome,
00:19:19.24 and its loss determining the inactive chromosome.
00:19:24.26 Now, what we also demonstrated in these early studies
00:19:27.15 is that we can genetically manipulate
00:19:30.15 the choice decision
00:19:32.02 by simply removing Tsix from one X chromosome.
00:19:35.00 And when we do that,
00:19:36.21 that chromosome is always the one
00:19:39.07 that becomes inactivated.
00:19:41.01 So, we can influence and manipulate which X chromosome
00:19:43.11 will become the inactive one.
00:19:47.28 So, then, what I told you is that
00:19:50.29 normally cells can choose
00:19:53.20 either one or the other X chromosome for inactivation.
00:19:56.21 But very strangely,
00:19:59.01 when we delete both copies of Tsix
00:20:01.27 -- not just one, but both copies of Tsix --
00:20:04.14 we see these additional cell types,
00:20:07.08 where both X chromosomes are inactivated
00:20:10.13 or neither X chromosome is inactivated.
00:20:16.18 So, it appeared to us here that the cells
00:20:20.29 are undergoing some kind of a chaotic choice.
00:20:23.07 Or maybe there's no choosing at all.
00:20:24.26 You see all combinations as a result of losing this antisense repressor.
00:20:29.20 So, this is a loss of mutually exclusive choice.
00:20:32.24 And from that, we postulate that
00:20:35.26 maybe there has been a loss of communication
00:20:38.26 between the two X chromosomes,
00:20:40.20 such that now cells.
00:20:42.21 you know, really, the left brain doesn't know what the right brain is doing,
00:20:45.14 going back to the analogy I drew in the first lecture.
00:20:49.19 So, these experiments also tell us that
00:20:52.23 the Tsix repressor is very important for that communication
00:20:56.08 between the two chromosomes.
00:20:58.19 Now, around the same time,
00:21:00.05 we and the Heard lab made an interesting observation,
00:21:03.27 which is that prior to X inactivation
00:21:08.24 the X. two X chromosomes behave like they're not even aware of each other.
00:21:12.00 But at the onset of X inactivation,
00:21:13.28 one of the very first things that we see is that the chromosomes come together,
00:21:16.12 and they briefly touch,
00:21:18.07 just at the X inactivation center.
00:21:20.05 And it's very brief.
00:21:22.03 It happens probably in under 15 minutes,
00:21:24.03 but let's say under 30 minutes.
00:21:25.23 And then when they come apart again,
00:21:27.20 one X chromosome is the active one
00:21:29.16 the other one is expressing Xist,
00:21:31.06 so it's become the inactive one.
00:21:32.27 It's almost as though the cells have flipped on a bistable switch
00:21:35.26 as a result of pairing.
00:21:37.13 And you can see this pairing event, here,
00:21:39.21 by DNA fluorescence in situ hybridization,
00:21:42.10 where you see two dots of the Xic
00:21:45.11 coming close together in a certain timeframe
00:21:48.01 during X inactivation.
00:21:49.17 And so, because of this observation,
00:21:51.14 we propose that the XX pairing process
00:21:55.06 may serve as a bridge by which the two chromosomes
00:21:57.28 can communicate with each other
00:22:00.19 prior to the choice decision.
00:22:05.05 So, in support of that idea, here.
00:22:08.14 which we've shown.
00:22:10.27 that the center responsible for pairing
00:22:14.04 is the same region that's responsible for allelic choice.
00:22:18.21 It's the same white bar that you show.
00:22:20.22 that you saw a few slides earlier.
00:22:23.15 So, this is a 15 kilobase region.
00:22:25.11 And intriguingly,
00:22:27.25 if we were to take this white line
00:22:30.03 -- take this genetic region --
00:22:32.13 and insert that into an autosome, far away,
00:22:35.23 that autosome is now induced
00:22:39.04 to pair with the X chromosome.
00:22:40.19 So, this region, this very, very small region,
00:22:43.10 is both necessary and sufficient
00:22:45.28 to direct pairing.
00:22:49.24 So, here are some real-life experiments.
00:22:51.21 When we delete both copies of Tsix,
00:22:54.11 the chromosomes no longer pair.
00:22:57.02 And as I mentioned,
00:22:59.09 there's a loss of mutually exclusive choice.
00:23:01.27 On the other hand,
00:23:04.11 if we insert extra copies of the pairing region into an autosome,
00:23:07.26 which is shown here in blue,
00:23:09.28 that autosome does something very strange,
00:23:12.19 which is that it attracts one of the X chromosomes.
00:23:16.11 one of the X chromosomes to come and pair with it,
00:23:19.01 and in doing so it prevents the two X chromosomes
00:23:23.15 from interacting with each other,
00:23:25.16 and X inactivation is arrested.
00:23:28.29 And so what these experiments tell us
00:23:31.17 is that XX pairing is very important
00:23:33.21 to somehow properly initiate X chromosome choice.
00:23:38.24 So, we propose that pairing is a mechanism
00:23:41.20 by which the two X chromosomes
00:23:44.09 can break their epigenetic symmetry.
00:23:47.26 So, prior to the onset of X inactivation,
00:23:50.26 Tsix is expressed from both X chromosomes.
00:23:54.05 And then the process of pairing results in the loss of antisense expression
00:23:59.28 from one X chromosome,
00:24:01.19 and it is from that chromosome that Xist becomes upregulated.
00:24:05.08 And on the opposite X chromosome,
00:24:07.11 Tsix persists,
00:24:09.19 and that blocks the upregulation of Xist,
00:24:12.13 allowing this chromosome to remain
00:24:15.24 active in the female cell.
00:24:17.26 So, we propose, then, that XX pairing
00:24:21.09 is a mechanism of crosstalking
00:24:23.17 which allows the two chromosomes
00:24:25.25 to adopt mutually exclusive fates,
00:24:28.13 of active and inactive X chromosome.
00:24:31.28 So, we've also observed that CTCF,
00:24:35.29 this very versatile zinc finger transcription factor,
00:24:38.28 is essential for X chromosome pairing,
00:24:42.08 by serving as an inter-chromosomal glue.
00:24:44.23 So, in these complicated experiments,
00:24:47.06 what you can see is that
00:24:49.18 CTCF binds to Tsix and Xite RNA,
00:24:51.29 and CTCF also binds to the DNA
00:24:54.25 -- that white line, that 15 kb region I demonstrated before --
00:24:58.15 to specific regions of the pairing and choice center.
00:25:04.23 So, this binding to the RNA
00:25:07.02 is essential for CTCF
00:25:10.04 to be recruited as an inter-chromosomal glue.
00:25:12.24 So, before concluding this lecture,
00:25:16.12 I would like to demonstrate what we think
00:25:20.07 is taking place during that process of allelic choice.
00:25:25.20 So, prior to the onset of X inactivation,
00:25:28.21 this pluripotency factor, OCT4,
00:25:31.24 binds to both Tsix and Xite,
00:25:34.13 and transactivates the expression of Tsix and Tsix.
00:25:38.18 So, I didn't mention that in my lecture,
00:25:40.26 but this is the case.
00:25:42.29 And then the expression of Tsix and Xite
00:25:45.05 recruits CTCF to this pairing region.
00:25:50.15 At the onset of X inactivation,
00:25:53.13 what we see is that the two chromosomes come together
00:25:56.24 and pair exclusively through this 15 kilobase region.
00:26:01.08 And we believe that this pairing event
00:26:03.22 serves as a platform
00:26:06.19 on which the two X chromosomes can communicate with each other,
00:26:09.12 and make the determination of
00:26:12.23 who will be the active versus the inactive x chromosome.
00:26:15.18 Now, exactly what they're saying to each other
00:26:17.27 and how this is done
00:26:19.21 is something that's under very active investigation.
00:26:22.19 We do not presently know.
00:26:24.12 However, we suspect that what happens is that
00:26:27.23 when the two chromosomes come apart again,
00:26:30.16 these transcription factors
00:26:33.08 -- like CTCF, and very likely many other factors --
00:26:35.11 will repartition onto one X chromosome.
00:26:38.26 And so CTCF is serving as a transcriptional repressor.
00:26:42.29 Its binding to this chromosome
00:26:46.06 will downregulate expression of Tsix as well as Xite.
00:26:51.04 And their downregulation is what allows
00:26:53.23 Xist to be upregulated from that chromosome.
00:26:57.08 And that chromosome becomes the inactive X.
00:27:00.06 But on the other hand,
00:27:01.29 on the future active chromosome,
00:27:03.15 Tsix and Xite persist,
00:27:05.13 and their persistence
00:27:08.28 prevents Xist from becoming upregulated,
00:27:10.15 and that chromosome remains an active chromosome.
00:27:17.20 So, before concluding Lecture 2, then,
00:27:20.05 I just want to mention one last thing,
00:27:22.20 which is that the ends of the sex chromosomes
00:27:27.00 -- the telomeres --
00:27:29.11 play a very important role during XX pairing.
00:27:33.07 Now, XX pairing is not taking place
00:27:35.27 in a random place in the nucleus.
00:27:38.00 Instead, it's taking place within what we call a tetrad, okay?
00:27:42.16 So, what we've now shown is that
00:27:45.04 the ends of both sex chromosomes
00:27:46.29 -- the X and Y --
00:27:49.26 produce a non-coding RNA called PAR-TERRA.
00:27:53.12 And PAR-TERRA agglomerates.
00:27:58.03 this RNA brings the two telomeres together.
00:28:00.01 both X chromosomes,
00:28:01.15 and even the X and Y chromosomes.
00:28:02.26 It brings the two sex chromosomes together
00:28:05.02 at the nuclear envelope.
00:28:06.14 And then that RNA serves as a tether,
00:28:08.12 and reels in the X inactivation center
00:28:11.28 so that pairing takes place within this tetrad
00:28:15.19 of two telomeres and two inactivation centers.
00:28:20.13 And you can see real-life examples, here,
00:28:22.24 by DNA FISH,
00:28:24.20 where a pair of the telomeres, shown in red,
00:28:29.07 and a pair of inactivation centers, shown in green,
00:28:32.07 have agglomerated at the nuclear envelope
00:28:35.03 to enable XX pairing.
00:28:37.17 So, why would they even bother to do this?
00:28:39.17 Well, because the nucleus is a vast space.
00:28:43.04 And it would take time for the two inactivation centers.
00:28:45.24 a lot of time for the two inactivation centers to come together.
00:28:49.05 And so this tethering mechanism
00:28:52.23 facilitates this homology searching process
00:28:56.11 through this process that we called a constrained diffusion
00:28:58.19 in 3-dimensional space.
00:29:01.04 So, that then concludes the second lecture.
00:29:05.21 And we will talk about
00:29:08.20 the initiation and spreading of X inactivation in Lecture 3.
The REU application deadline is: January 31st, 2017.
There are five items required to complete an REU application:
- REU Student Application Form
- A Letter of Recommendation from an On-Campus Mentor
- A Letter of Recommendation from a Faculty Member
- Official Transcript(s)
- Letter certifying your membership to a LSAMP program at your home institution
1. REU Student Application Form (Word document 135 kb) (includes Statement of Purpose)
Click on the application link above and open the MS Word application file. Upon opening the document, please click in the blank areas of each field and insert the appropriate application information. For REU project preferences, please select mentors/projects from the list available under “Downloads” on the right sidebar of this website. OTS has two REU program research sites: La Selva and Las Cruces. Please make sure you select your preference (OTS will take this information into consideration when defining the REU groups).
After you complete the first two pages of the general application, you will need to write the ‘Statement of Purpose’, which is on the third page.
Please save your application using the following format:
REUappl(YOUR LASTNAME, YOUR FIRST INITIALS).doc
For example, if your name is Jane Elizabeth Smith, you should label your application:
After the application has been completed and saved, please send it as an attachment to:
2. Two Letters of Recommendation
Science Faculty Member ( Word document 97 kb) – Two letters of recommendation are required from two science faculty members who knows you well, are from your major department, and with whom you have taken at least one class within the past two years. You must download this form and send it to each professor who is writing your recommendation. Instructions of how he/she is to submit the form are included within the document.
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OTS REU – Undergraduate Program
Organization for Tropical Studies
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*** Should you have any questions about the program or how to apply, please contact Kattia Mendez, Undergraduate Program Assistant at the OTS Costa Rican Office, at: [email protected] .
Biology major update: New offices, new structure, expanded advising team
The UW-Madison biology major is operating under a new administrative structure, in a new location, with additional staff and a new website. Biology is the most popular major on campus, with 1,372 students enrolled this fall—798 in CALS, 574 in L&S and other schools and colleges—and 62 faculty mentors in 30 departments across campus (details below).
The program is now being managed jointly by CALS (through the Department of Bacteriology) and L&S (through the Department of Zoology). There’s also a newly appointed program committee, co-chaired by Professors Donna Fernandez (Botany) and Heidi Goodrich-Blair (Bacteriology).
Most important, there is a an expanded biology major advising team:
- Mary Smith, senior student services coordinator, has been an administrator and advisor for the biology major since 2003.
- Brian Asen, student services coordinatorfor the biology major since 2011. After earning a degree in Education, Brian came to UW-Madison in 2003 to work as a Graduate Coordinator in the Department of Computer Sciences. In 2006 he became a program coordinator in the Institute for Biology Education, where he coordinated research programs for both undergraduate and pre-college students (the Integrated Biological Sciences Summer Research Program, PEOPLE and the Summer Science Institute). Since joining the biology major two years ago, Brian has enjoyed advising many biology students as they navigate their way through their undergraduate careers.
- Todd Courtenay, student services coordinator, comes to CALS from the College of Engineering where he was an advisor in the EGR office. Prior to professionally advising students, he worked with undergraduates as a lecturer and teaching assistant while a graduate student at UW-Madison. With an academic background in history of science, international studies and geography, Todd is excited to continue working with STEM students and helping them navigate the breadth of opportunities at UW-Madison. He is looking forward to the continued development of the Biology major, and is especially passionate about international opportunities for STEM students and facilitating undergraduate research opportunities. Originally from Madison, Todd earned a BA in International Studies at the University of Oregon and a PhD in Geography at UW-Madison.
- Darby Sugar, student services coordinator, comes to the Biology Major Advising team after working within the science realm since 2003 at Kraft Oscar Mayer, UW-Madison, Lucigen and Madison College. Darby received her BS from the University of Arizona and her MS in Bacteriology from UW-Madison. She is excited to return to UW and to the same building where conducted her graduate research. She is looking forward to working with her advisees and helping each individual student find their unique path.
- Kelley S. Harris-Johnson, Biology Program Manager, joins the Biology Advising team after working in the Department of Biochemistry as an Assistant Faculty Associate where she taught and developed undergraduate courses and led student services initiatives. She is eager to continue advising and mentoring students and to provide administrative and managerial oversight for the biology major. She will work closely with the faculty co-directors and the Program Committee to establish and execute the vision for the Biology Program. Kelley earned a BS in Biology from Xavier University of Louisiana and a PhD in Genetics from the UW-Madison.
Biology students are also guided by faculty mentors across campus:
Inventors of Tomorrow
Today’s themes were Wind, Balloons, and Flight. These could be combined in one session, or split into two or three classes.
Question of the Day: What can the wind blow around?
Sorting activity – Can the Wind Move It? On a big table, or on the floor, put out ways to create a breeze, such as bellows, paper fans, balloon pumps, hair dryers and straws to blow through. Then put an assortment of objects out. Have children try blowing the objects around the table. For young kids (age 3 – 4), put out two bowls to sort into, labeled “Blows in the Wind” and “the Wind Can’t Move It”. Put out heavy objects the wind obviously can’t move, and light ones that it can. For older children, put out three bowls “Easy to Move with Wind”, “Hard to Move with Wind” and “Didn’t Move” and a wide variety of objects. They’ll discover that, in general, lightest weight things are easiest to move, heavier things are harder, and heavy things don’t move. But, the strength of the wind matters, and the shape of the object matters. (source)
Playing with Fans: Set up a fan and put scarves or streamers or balloons or other lightweight objects out so the children can hold them up, see them blow in the wind, then let go and watch them flutter away. Optional: put out objects that are too heavy for the air from the fan to lift so they can discover that.
We also have some specialized equipment that we used in this class:
- the scarf cannon (click on that link to learn how to build your own). We aimed the tube straight up at the ceiling so the scarves shot straight up and out, or you could float a lightweight plastic ball on the current of air.
- the wind tube (see video below. Tutorial for how to build one is here). There’s endless fun in testing out various items in the tube: we tested paper cups – didn’t float on the air current, but would roll around in circles on the surface of the fan snow cone cups will float – if you turn them upside down scarves shoot out the top, then flutter to the ground, making them fun to catch we have a little plastic Frisbee that never escapes – it just bangs around inside the tube. My favorite is food trays (what we call “snack boats”). Not only do they float on their own – but even better, you can put toys inside of them that are too heavy to float, but the boat catches the air so well that it can carry those toys up.
- We also had kids build paper “wind tube flyers” using designs we found at the Orlando Science Museum.
- – we found this at a garage sale. It works sort of like a mini wind tube, but it’s a REALLY weak fan, so it barely floats out the fabric butterflies
Craft – Sailboats. We made sailboats using corks from wine bottles, rubber bands, popsicle sticks and stiff plastic sails. Read about my design process and see the “how to” tutorial here.
Water table: We filled a water table, then gave each kid a straw (labelled with their name) so they could use the straw to blow their sailboat around the water.
Building Project: We also put out the Duplo pinwheel kit, which encourages children to try following directions to build a pre-designed project, and a few toy pinwheels for children to explore.
Group art project: The blustery day collage. Teacher Cym painted a large picture of a tree with some swirls and spirals to indicate the wind blowing across it. The kids glued on dried leaves, feathers, other things that would swirl in the wind. [option: you could ask the children things like – “should we glue a brick on the picture? Or rocks? No? Why not?” and explore the idea of what blows in the wind and what does not.]
Easy crafts: Teach how to accordion fold a fan out of paper. Cut a spiral of paper so it becomes a wind spinner. (we tested these in the wind tube too…)( http://www2.scholastic.com/content/images/articles/m/msb_stormprint.gif
Books to read: We read and Face the Wind by Cobb, which is one of the best non-fictions for this 3 – 7 year old age group that I have read! Just a really nice combination of readable text, nice illustrations, clear concepts, examples that are familiar to kids, and ideas for experiments kids can do. (I did skip a few of these ideas when reading out loud, both for sake of time, and because it can be hard for kids to resist wanting to try every experiment they head a book describe, and we weren’t going to be doing all of them. (After reading it, I looked up all the other books by Cobb, and added many to our curriculum. Vicki Cobb has a video here where she talks through why she wrote this book the way she did, and offers teachers/parents more information which can help enhance their read-aloud of the book.)
Other options: Wind by Bauer is a simple non-fiction book about wind. Feel the Wind by Dorros also looks like a good option. Mouse’s First Spring , or one of the many story books out there about things getting swept away in the wind. Other ones I’d like to check out include Like a Windy Day and the Fantastic Flying Books . Some others I’ve heard recommendations for are: Aesop’s Fable about the Sun and the Wind, One Windy Wednesday, Someone Bigger (about a kite), Frog and Toad – the Kite, Who Took the Farmer’s Hat, Gilberto and the Wind, Millicent and the Wind.
Balloons : The only balloon activity we did in this class session was that we got helium balloons, and we tested to see how much weight the balloons could lift. There’s lots more balloon activities in this post.
Kites: We built simple kites with paper and bamboo skewers. This is definitely an adult-assistance project for kids. We then tried flying them outside, but didn’t have enough wind that day. (Here are directions for lots of kites… http://teacherbulletin.ehclients.com/media/resources/V09-6_KITE_making_PLANS.pdf)
Paper Airplanes! You can put out books with ideas of how to fold them, or print designs from www.funpaperairplanes.com/, or create a template where all they need to do is fold along the lines. Or just put out paper, and let the parents re-live their childhood hobbies.
Gliders. Cut strips of index cards or paper. Tape them to make two rings – one big and one small. For example, a 4 inch strip and a 6 inch strip. Tape one to one end of a straw, and the other to the other end. Hold it up and throw it like a paper airplane.
Straw Rockets : Take a piece of paper, and fold it around the top third of a straw. Fold over the top and tape it closed. It wants to fit well, but not too tightly. Then you blow into the straw and the rocket shoots through the air. Simple Play Ideas has a super simple version of this. Buggy and Buddy has a template for a fancier art project version. JPL NASA has the most science-y version, for older kids with good dexterity.
"Understanding arrhythmogenic cardiomyopathy using human induced pluripotent stem cells"
Jared Churko, PhD, is an assistant professor at the University of Arizona within the Department of Cellular and Molecular Medicine. He received his PhD in anatomy and cell biology from Western University and trained as a postdoctoral fellow at Stanford University within the Cardiovascular Institute. His lab seeks to understand the mechanisms leading to heart disease by combining single cell transcriptomics, systems biology, stem cell biology, genetic engineering, and bioinformatics. Specifically, his lab utilizes human induced pluripotent stem cells (hiPSC) to generate cardiac cell types and develops tools for precision and regenerative medicine. He is appointed as the director of the University of Arizona iPSC Core.
During his talk, he will discuss the current state in using hiPSCs for heart disease modelling. Specifically, his talk will describe his recent progress in generating hiPSCs from patients with arrhythmogenic cardiomyopathy, performing a transcriptomic analysis of cardiomyocytes derived from patient specific iPSCs to identify disease specific mechanisms, and performing organoid and functional assays to model arrhythmogenic cardiomyopathy in a dish.
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Genspace is the world’s first community biology lab — a place where people of all backgrounds can learn, create, and grow with the life sciences.
Since 2009, we have served the greater New York area by providing hands-on STEAM education programs for youth and adults, cultural and outreach events for the public, and a membership program to support New York’s community of creatives, researchers, and entrepreneurs. Our programs demystify scientific processes, provide a platform for innovation, and cultivate the next generation of life sciences leaders in emerging global technologies, such as biotechnology, neuroscience, epidemiology, genomics, and many more.
Watch the video: Γιατί να σπουδάσω βιολογία; επιστήμη ΤΣΑΚ ΜΠΑΜ #9 (August 2022).