A researcher pulls a frozen vial of human embryonic stem cells at the University of Michigan Center for Human Embryonic Stem Cell Research Laboratory in Ann Arbor, Mich., in this Oct. 22, 2008 file photo. The face of science, writes Kristin Baetz, should be changing, and here's how to do it. Paul Sancya, THE ASSOCIATED PRESSPaul Sancya / THE ASSOCIATED PRESS

At science meetings, women need to grab the mic and not let go.

As the director of the Ottawa Institute of Systems Biology at uOttawa and as past-president of the Canadian Society for Molecular Biosciences, I get a lot of emails asking me to attend or help advertise science conferences.

Most of these emails end up in my delete file.

Why? I am no longer going to promote, sponsor or attend meetings that do not have a significant number of female speakers.

If accomplished female scientists are not asked to present at meetings, by default it suggests their research is not as exciting or as good as that of their male colleagues.

This matters both financially and professionally your speaking portfolio contributes to the success of grant applications and whether one receives tenure or becomes a full professor.

Canada needs equity in science, technology, engineering and mathematics (STEM). As Imogen Coe, dean of science at Ryerson University and a leading expert in the barriers of women in STEMs, states, If we are to solve or even address the complex problems that we face, we need all hands on deck, we need everyone at the table, we need to leverage all the human potential and intellectual capacity that is available to us.

With women comprising more than 50 per cent of trainees and early-career researchers in biomedical fields, how is it that that the problem of #YAMMM (yet another mostly-male meeting) still exists?

The answer is this: Scientists let it happen.

Consider how science conferences are run. For a number of reasons, largely mid- or late-career scientists organize meetings, and they are often men. Only established researchers, who are no longer struggling to build their research programs, build new courses or possibly to raise young families, have the time to organize meetings.

Its only human that when they solicit speakers, its colleagues they know, or want to collaborate with. If you are an early-career researcher, especially female, many meeting organizers might not have you on their radar.

This will change when organizers of meetings including scientific societies and funders start demanding that equity is a fundamental requirement of meetings.

Coe recently challenged me to ensure that the speakers at our 2017 Canadian Society for Molecular Biosciences meeting reflected our attendees. I am both proud and ashamed to announce that at our 60th annual science meeting, 50 per cent of our speakers were female.

I insisted that our organizers seek out exceptional female speakers to give plenary talks.

While this was embraced by many of my colleagues, it was strongly resisted by others. Some refused to even consider equity issues when selecting speakers. Why? One often-made excuse is that there are no excellent females in a field to invite.

Jodi Nunnari, president-elect of the American Society for Cell Biology, calls this a poor excuse, which justifies the same old status quo. To counter this argument, her society established a speaker referral list to identify outstanding women scientists across the field of cell biology.

Heres what happened at our meeting. Many back-handed comments were made about how different the speaker lineup was. I got upset emails over not being asked to give a talk. One said, I guess I didnt tick-off the right boxes.

These reactions consistently originated from mid- and late-career male scientists.

However, for every negative comment, I received tenfold more positive comments from across the research spectrum, from trainees to retired professors, both male and female.

While I am hopeful that our government will one day tackle the equity issues in STEM by directly tying it to funding, scientists cannot just wait. As individuals and as institutions we have the ability to literally change the face of conferences and success in Canadian science.

Lets commit to ending the #YAMMM.

Kristin Baetz is the director of the Ottawa Institute of Systems Biology and professor at uOttawa.

Read the original:
Baetz: Standing up for female scientists and researchers - Ottawa Citizen

The force gravity and physical activity put on our bones causes tiny tears in the membranes of the tiny cells that enable us to make or break down bone, scientists say. Pictured are Drs. Meghan E. McGee-Lawrence and Paul McNeil. Credit: Phil Jones, Senior Photographer, Augusta University

The force gravity and physical activity put on our bones causes tiny tears in the membranes of the tiny cells that enable us to make or break down bone, scientists say.

While that may sound bad, it's actually a key piece of how the force we put on our bones helps keep them strong, they report in the Journal of Orthopaedic Research.

"The bone has to constantly adapt and make sure that is has the right design to withstand the loads you are going to put it through," says Dr. Meghan E. McGee-Lawrence, biomedical engineer in the Department of Cellular Biology and Anatomy at the Medical College of Georgia at Augusta University.

Osteocytes manage the osteoblasts that make bone as well as the osteoclasts that break bone down and were known to sense mechanical loading, but just how they sensed load was unknown.

McGee-Lawrence and MCG cell biologist Dr. Paul McNeil are the first to find the small tears in response to force exacted by walking up the stairs or lifting weights.

Not only do the cells experience membrane tears but it's the highest number McNeil, an expert in cell membrane repair, has seen in a variety of cell types. "It's remarkable," says the study coauthor. And, the heavier the mechanical load, the more tears; for example the mice walking on a treadmill versus just moving about in their cage.

Better understanding the specific mechanism by which these cells sense then respond to mechanical load should enable identification of logical targets for improving the strength and health of aging bones as well as bones challenged by diseases like diabetes, says McGee-Lawrence the study's corresponding author.

Osteocytes are plentiful in bone and each has hundreds of tiny processes reaching out in every direction that help secure them to the bone matrix. McGee-Lawrence likens their look to a sweetgum ball. She and McNeil have early evidence the diminutive cells and their projections are both very vulnerable to tearing and that vulnerability appears to make them a natural for responding to mechanical load.

Once tears happen to cell membranes, more calcium rushes inside the cells. This mineral closely associated with bone health and present outside the cell at concentrations 10,000 times higher than inside the cell, was known to be an initiating signal, McNeil says. His work has shown how in many cell types including now osteocytes, the load causes the tears which allows calcium to rush in to both rapidly heal tears and to set in motion inside a host of actions that, in this case, remodels bone.

In cell cultures, they watched as increased calcium levels inside osteocytes triggered an increase in the production of the protein c-fos. The protein also is well-studied and known to be involved in the signaling pathways that lead to stronger bones in response to exercise, but c-fos' connection with membrane tearing was another unknown.

Osteocytes use their micron-thin tentacles to communicate with each other and the scientists also learned that when one osteocyte gets tears, it appears to communicate its load to neighboring osteocytes so the calcium level goes up in those as well even without a tear. The message the torn osteocyte shares it to tell osteoblasts to make the bones stronger and the osteoclasts to quit breaking bone down.

The idea of further shoring up bone is likely to be better prepared for whatever mechanical load comes next, McGee-Lawrence says.

Conversely, the lack of loading and subsequent tearing may be why astronauts' bone and muscle weaken in zero gravity, McNeil says.

McGee-Lawrence is principal investigator on a new $450,000 National Science Foundation grant that will help them further parse this important puzzle and the potential for enabling better bone health with age and disease.

"We are wondering if bone loss with aging is due to osteocytes becoming more fragile or less able to repair as we age," say McNeil, co-investigator on the ongoing studies. "If they do, you would lose them over time and, in fact, we know you do lose them."

Part of what they are doing with the new grant includes looking at mice with a genetic deficiency in cell membrane repair. They want to see if the 50-year-old drug poloxamer 188, which was designed to reduce the thickness of blood, is found in products like toothpaste and has been shown to repair other cell membranes, might help osteocytes remain proficient at responding to mechanical load. Like many of our senses that dull with age, aging osteocytes don't sense critical mechanical loads as well.

"It's a way you can influence membrane repair rates so if we speed up how fast that tear repairs, is that going to influence the osteocytes?" McGee-Lawrence says. They'll also look at the impact of slowing repair down.

No drug on the market for osteoporosis is known to enhance osteocyte sensitivity.

"We are starting to understand why calcium signaling gets initiated in wounded cells and then that gives us a mechanism we can target to try to influence how well bone detects mechanical loading," McGee-Lawrence says.

Disease may also complicate the common action of cell membrane tear and repair. For example, McNeil has shown diabetes, which is associated with bone loss, can lead to problems with membrane repair of other cell types. Now the MCG scientists are looking at whether it similarly affects osteocytes.

Bone and muscle health are inextricably connected and McNeil has done pioneering work that shows one way we keep our muscles strong and even increase their size is through this process of tear and repair in the membrane of muscle cells.

"If you go to the gym and exercise your muscles, they are going to get bigger and stronger and at the same time if you sit around all day your muscles are going to get weaker," McGee-Lawrence says. "Bone does the same thing." McNeil notes the difference between the right and left hands and arms of a right-handed tennis player.

"This bone is full of cells. Some are building new bone, some are breaking down bone and it is constantly being remodeled," McNeil adds, holding up a large muskox bone.

People hit their peak bone mass in the late 20s or early 30s. After that, the percentage of osteoblasts to osteoclasts starts to shift so that you are slowly losing rather than building bones. Active youth, they note, tend to build a better bone mass that should comfortably see them into old age, particularly if they remain active.

Failure of rapid membrane repair is associated with weaker muscles even muscle disease, they note, and the scientists expect the same also holds true in bone. Future studies include exploring whether repair failure contributes to common problems like osteoporosis.

Explore further: Research identifies how master regulator, bone-building protein can be used for therapy

Go here to read the rest:
Tears in tiny bone cells called osteocytes appear an important step to better bones - Medical Xpress

ByTaylor Jade Powell

Oscar, Cristian, Luis, and Lorenzo were never expected to amount to much. Born in Mexico and growing up in Arizona, the four undocumented teenagers were poor and attending an underfunded high school in the desert.

Though the students had never seen the ocean, two science teachers inspired them to build an underwater robot and compete in a marine robotics competition at the University of California, Santa Barbara.

Spare Parts: Four Undocumented Teenagers, One Ugly Robot, and the Battle for the American Dream tells the stories of young men with insurmountable odds stacked against themdeportation, prejudice, and a robotics team with 10 times more funding.

The book by Joshua Davis addresses the issue of immigration and challenges students to consider alternate ways of learning, said Tiffany Sanchez, Johns Hopkins University's interim dean of student life. That's why the Common Read Committee chose it as this year's assignment for the Class of 2021.

New students will discuss the book in small groups led by faculty, staff, resident assistants, and first-year mentors today as part of orientation.

"We hope this makes Hopkins feel a bit more like home and introduces new students to people and ideas that they might not normally come in contact with," Sanchez said.

Tiffany Sanchez

Interim dean of student life

The Common Read program started in 2007 with a mission to bring together first-year class members and new transfer students, while encouraging critical thinking and intellectual discussion. Each year a committee made up of JHU staff and faculty chooses a book that students receive via mail.

Over the summer, students had the opportunity to submit essays or short videos in response to the book, and this year there were more than 70 contest entries. Winners will be honored at the Common Read Keynote on Sept. 7, where protagonists Fredi Lajvardi and Oscar Vazquez will talk about their experiences depicted in the novel.

"It's such a great way to get to know our new students, and I enjoy learning about their lives," Sanchez said. "Each response reminded me that there are over 1,300 new individuals in our community and each of them comes with their own experiences, values, and ideas about the world."

One of three winners is Kelechi Nwankwoala, an incoming Writing Seminars and molecular cell biology double-major. In his contest submission, Nwankwoala said he considered his parents' immigration to America and his own fears of being treated differently because of his race as part of his response to the book.

"I tried to use narrative to express how racial prejudice and fear can become a constant weight on the psyche," he said. "It is my belief that constant fear does something to people; it effects the way you interact with the world. I wanted to illustrate how my own fears have changed over the years and how I have become more and more aware of the weight I shoulder."

Original post:
Something in common: New JHU students discuss shared summer reading assignment, 'Spare Parts' - The Hub at Johns Hopkins

Binding of steroid estrogen hormones to estrogen receptor (ER) in the cell nucleus triggers the sequential recruitment different coactivators to regulate gene transcription.

Estrogen hormones regulate gene expression. They achieve this by first binding to estrogen receptor in the cell nucleus, which triggers the recruitment of different molecules called coactivators in specific order. In a study published in Molecular Cell, a team of researchers at Baylor College of Medicine, the University of Texas MD Anderson Cancer Center and the University of Texas Health Science Center at Houston shows that the sequential recruitment of coactivators is not simply adding molecules to the complex, it results in dynamic specific structural and functional changes that are necessary for effective regulation of gene expression.

Estrogens are a group of hormones that are essential for normal female sexual development and for the healthy functioning of the reproductive system. They also are involved in certain conditions, such as breast cancer. Estrogen also plays a role in male sexual function. Estrogens carry out their functions by turning genes on and off via a multi-step process. After estrogen binds to its receptor, different coactivators bind to the complex in a sequential manner.

Experimental evidence suggests that different estrogen-receptor coactivators communicate and cooperate with each other to regulate gene expression, said corresponding author Dr. Bert OMalley, chair and professor of molecular and cellular biology and Thomas C. Thompson Chair in Cell Biology at Baylor College of Medicine. However, how this communication takes place and how it guides the sequence of events that regulate gene expression was not clear.

In this study, OMalley, Dr. Wah Chiu, Distinguished Service Professor and Alvin Romansky Professor of Biochemistry and Molecular Biology at Baylor during the development of this project, and their colleagues combined cryo-electron microscopy structure analysis and biochemical techniques and showed how the recruitment of a specific coactivator CARM1 into the complex guides the subsequent steps leading to gene activation.

For the estrogen receptor complex to be able to regulate gene expression, the coactivator CARM1 needs to be added after other coactivators have been incorporated into the complex, said first author Dr. Ping Yi, assistant professor of molecular and cellular biology at Baylor. We discovered that when CARM1 is added, it changes the complex both chemically and structurally, and these changes guide subsequent steps that lead to gene activation.

We now have a better understanding of how this molecular machine works and of what role each one of the components plays. We are better prepared to understand what might have gone wrong when the machine fails, OMalley said.

Other contributors to this work include Zhao Wang, Qin Feng, Chao-Kai Chou, Grigore D. Pintilie, Hong Shen, Charles E. Foulds, Guizhen Fan, Irina Serysheva, Steven J. Ludtke, Michael F. Schmid, Mien-Chie Hung and Wah Chiu.

Support for this study was provided by the Komen Foundation (5PG12221410), the Department of Defense (R038318-I and W81XWH-15-1-0536); National institutes of Health grants (HD8818, NIDDK59820, P41GM103832 and R01GM079429); CNIHR, R21AI122418 and R01GMGM072804; CPRIT grants (RP150648 and DP150052); and a National Cancer Institute Cancer Center Support grant (P30CA125123) to the BCM Monoclonal Antibody/recombinant Protein Expression Core Facility.

Read more from the original source:
Research reveals how estrogen regulates gene expression | Baylor ... - Baylor College of Medicine News (press release)

Adult stem cells can be extracted from human fat. Patrick T. Fallon /The Washington Post/Getty Images hide caption

Adult stem cells can be extracted from human fat.

The Food and Drug Administration is cracking down on "unscrupulous" clinics selling unproven and potentially dangerous treatments involving stem cells.

Hundreds of clinics around the country have started selling stem cell therapies that supposedly use stem cells but have not been approved as safe and effective by the FDA, according to the agency.

"There are a small number of unscrupulous actors who have seized on the clinical promise of regenerative medicine, while exploiting the uncertainty, in order to make deceptive, and sometimes corrupt assurances to patients based on unproven and, in some cases, dangerously dubious products," FDA Commissioner Scott Gottlieb said in a statement Monday.

The FDA has taken action against clinics in California and Florida.

The agency sent a warning letter to the US Stem Cell Clinic of Sunrise, Fla., and its chief scientific officer, Kristin Comella, for "marketing stem cell products without FDA approval and significant deviations from current good manufacturing practice requirements."

The clinic is one of many around the country that claim to use stem cells derived from a person's own fat to treat a variety of conditions, including Parkinson's disease, amyotrophic lateral sclerosis (ALS), and lung and heart diseases, the FDA says.

The Florida clinic had been previously linked to several cases of blindness caused by attempts to use fat stem cells to treat macular degeneration.

The FDA also said it has taken "decisive action" to "prevent the use of a potentially dangerous and unproven treatment" offered by StemImmune Inc. of San Diego, Calif., and administered to patients at California Stem Cell Treatment Centers in Rancho Mirage and Beverly Hills, Calif.

As part of that action, the U.S. Marshals Service seized five vials of live vaccinia virus vaccine that is supposed to be reserved for people at high risk for smallpox but was being used as part of a stem-cell treatment for cancer, according to the FDA. "The unproven and potentially dangerous treatment was being injected intravenously and directly into patients' tumors," according to an FDA statement.

Smallpox essentially has been eradicated from the planet, but samples are kept in reserve in the U.S. and Russia, and vaccines are kept on hand as a result.

But Elliot Lander, medical director of the California Stem Cell Treatment Centers, denounced the FDA's actions in an interview with Shots.

"I think it's egregious," Lander says. "I think they made a mistake. I'm really baffled by this."

While his clinics do charge some patients for treatments that use stem cells derived from fat, Lander says, none of the cancer patients were charged and the treatments were administered as part of a carefully designed research study.

"Nobody was charged a single penny," Lander says. "We're just trying to move the field forward."

In a written statement, U.S. Stem Cell also defended its activities.

"The safety and health of our patients are our number one priority and the strict standards that we have in place follow the laws of the Food and Drug Administration," according to the statement.

"We have helped thousands of patients harness their own healing potential," the statement says. "It would be a mistake to limit these therapies from patients who need them when we are adhering to top industry standards."

But stem-cell researchers praised the FDA's actions.

"This is spectacular," says George Daley, dean of the Harvard Medical School and a leading stem-cell researcher. "This is the right thing to do."

Daley praised the FDA's promise to provide clear guidance soon for vetting legitimate stem-cell therapies while cracking down on "snake-oil salesmen" marketing unproven treatments.

Stem-cell research is "a major revolution in medicine. It's bound to ultimately deliver cures," Daley says. "But it's so early in the field," he adds. "Unfortunately, there are unscrupulous practitioners and clinics that are marketing therapies to patients, often at great expense, that haven't been proven to work and may be unsafe."

Others agreed.

"I see this is a major, positive step by the FDA," says Paul Knoepfler, a professor of cell biology at the University of of California, Davis, who has documented the proliferation of stem-cell clinics.

"I'm hoping that this signals a historic shift by the FDA to tackle the big problem of stem-cell clinics selling unapproved and sometimes dangerous stem cell "treatments" that may not be real treatments," Knoepfler says.

Go here to read the rest:
FDA Cracks Down On Stem-Cell Clinics Selling Unapproved Treatments - NPR

GETTY

The team of British researchers believe the groundbreaking method could shrink tumours and be more effective than any other existing treatments - such as chemotherapy.

The new process which kills off cancer cells has been called Caspase Independent Cell Death (CICD) and in trials led to the complete eradication of tumours in experimental models.

Scientists now believe the groundbreaking new research, published in Nature Cell Biology, could revolutionise the way cancer is tackled.

Lead author Dr Stephen Tait, from the University of Glasgow, explained: We were interested in identifying an alternative way to kill cancer cells. And weve identified a process called Caspase Independent Cell Death that appears, really excitingly, to be more effective (than other current methods).

Currently, most anti-cancer therapies - chemotherapy, radiation and immunotherapy - work by killing cancer cells through a process called apoptosis, which activates proteins called caspases, leading to cell death.

We were interested in identifying an alternative way to kill cancer cells

Lead author Dr Stephen Tait

But in apoptosis, therapies often fail to kill all the cancer cells, leading to disease recurrence, and can also have unwanted side effects that may even promote cancer.

The scientists at the University of Glasgow wanted to develop a way to improve therapy that induces cancer cell killing while also mitigating unwanted toxicity.

Announcing the successful new process, Dr Tait, also of the Cancer Research UK Beatson Institute, Institute of Cancer Sciences, said: Our research found that triggering Caspase-Independent Cell Death (CICD), but not apoptosis, often led to complete tumour regression.

Especially under conditions of partial therapeutic response, as our experiments mimic, our data suggests that triggering tumour-specific CICD, rather than apoptosis, may be a more effective way to treat cancer.

Unlike apoptosis, which is a silent form of cell death, when cancer cells die through CICD, they alert the immune system through the release of inflammatory proteins.

The immune system can then attack the remaining tumour cells that evaded initial therapy-induced death.

The researchers used lab-grown colorectal cancer cells to show the advantage of killing cancer cells via CICD, however, these benefits may be applicable to a wide-range of cancer types.

Getty Images

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How to prevent skin cancer

Dr Tait added: In essence, this mechanism has the potential to dramatically improve the effectiveness of anticancer therapy and reduce unwanted toxicity.

"Taking into consideration our findings, we propose that engaging CICD as a means of anti-cancer therapy warrants further investigation.

And he explained why it could be more effective than existing traditional treatments such as chemotherapy or radiotherapy.

He said: What we found in essence is the cells that undergo Caspase Independent Cell Death, they stimulate an immune response against the rest of the rumour.

In effect, you dont necessarily need to kill all the tumour cells with therapy because weve now elicited an immune response that then clears out the remaining tumour - in doing so eradicating the cancer.

GETTY

Latest figures show that half of all Britons born after 1960 will be diagnosed with some form of cancer during their lifetime.

Experts say four in 10 cancer cases are linked to lifestyle factors.

Smoking remains the largest single preventable cause.

More than half of cancer deaths in the UK are of people aged 75 years and over.

Last night, cancer research bodies in the UK gave the new research a warm welcome.

GETTY

Dr Justine Alford, Cancer Research UKs senior science information officer, said: Although many cancer treatments work by triggering apoptosis, that method sometimes fails to finish the job and instead may lead to the tumour becoming harder to treat.

And she added: This new research suggests there could be a better way to kill cancer cells which, as an added bonus, also activates the immune system.

Now scientists need to investigate this idea further and, if further studies confirm it is effective, develop ways to trigger this particular route of cell death in humans.

The new paper is published in Nature Cell Biology.

The paper was majority funded by Cancer Research UK.

Read the original post:
Cancer breakthrough: Scientists discovery new process which triggers death of cancer cells - Express.co.uk

Murine 2-cell stage embryo: L1 transcripts are visualized in white, DNA is shown in blue. Credit: Helmholtz Zentrum Mnchen

Retrotransposons are repetitive elements that form almost half of the mammalian genome. Even though they are so common, they have previously been considered to be fairly insignificant. Together with colleagues from the USA, scientists from the Helmholtz Zentrum Mnchen have now shown in Nature Genetics that retrotransposons play an important role in embryonic development.

The researchers specifically investigated the role of so-called LINE1 (L1) elements, the most abundant retrotransposon family in mammals. "We already knew L1 elements to be highly expressed in early embryogenesis and so we wanted to know if this transcription is important in the events taking place in the early embryo" says Prof. Dr. Maria Elena Torres-Padilla who headed the study. She is director of the Institute of Epigenetics and Stem Cells (IES) at Helmholtz Zentrum Mnchen and professor of Stem Cell Biology at the Ludwig-Maximilians-Universitt Mnchen (LMU).

"Critical for the development of the embryo"

Examining the expression of L1 in an experimental model, the researchers observed a peak when the embryo consists of only 2 cells, followed by a decrease in expression by the time the embryo attaches to womb of the mother. These stages are crucial for a successful pregnancy. To understand the importance of L1 elements they used artificially designed transcription factors (TALE, for transcription activator-like effector) to prevent or promote L1 expression in embryos. "We found that too much or too little L1 expression caused development to come to a halt" explains Dr. Joanna Jachowicz (IES), first author of the paper. "This means that the precise timing and level of retrotransposon expression is critical for the development of the embryo."

Unexpectedly, the scientists showed that the mechanism behind this regulation was independent of the coding nature of the transcript and of retrotransposition, that is, the ability of these elements to 'jump' to other parts of the genome. The researchers instead turned their attention to the chromatin. Using their engineering approach, the researchers showed that expressing L1 caused chromatin to be more open, while stopping L1 expression caused chromatin to be more tightly packed.

"These results identify a novel role for retrotransposons in shaping the chromatin 'landscape' necessary for the early developmental programme", explains Torres-Padilla. "It was previously assumed that the activation of retrotransposons was simply a side-effect of the chromatin remodelling occurring after fertilisation, a process termed epigenetic reprogramming. Our study demonstrates that L1 elements have a specific role in regulating chromatin accessibility which in turn is necessary for the correct developmental programme to take place. This study is hugely significant in assigning a role to a large amount of the mammalian genome at the very earliest stages of life."

In the future, the scientists would like to explore this process further and investigate whether other transposable elements have similar functions. "The overall aim of our research is to understand the processes occurring in the early embryo" adds Torres-Padilla. "This is a very fascinating stage of development because all the cell types of the body will arise from the single cell present after fertilisation". This is particularly relevant for the field of regenerative medicine, which aims to create different cell types and organs in the petri-dish for therapeutic use.

Explore further: From pluripotency to totipotency

More information: "LINE-1 activation after fertilization regulates global chromatin accessibility in the early mouse embryo," Nature Genetics (2017). DOI: 10.1038/ng.3945

Journal reference: Nature Genetics

Provided by: Helmholtz Zentrum Mnchen - German Research Center for Environmental Health

Read this article:
Repetitive elements shape embryonic chromatin landscape - Phys.Org

Royan International Twin Congress on Reproductive Biomedicine and Stem Cells Biology & Technology is a joint of two separate congresses with different themes held by Royan Research Institute Reproductive Biomedicine and Stem Cells Research Center.

The two joint events include the 18thCongress on Reproductive Biomedicine and 13thCongress on Stem Cell Biology and Technology scheduled for August 30- September 1, 2017.

Royan International Research Award winners, including five foreign and five Iranian researchers, will present their researchers on Reproductive Biomedicine and Stem Cell Biology & Technology during the Congress time.Each winner will be rewarded with a certificate, the symbol of Royan Award and a cash prize.

Main topics of the 18th congress on Reproductive Biomedicine include Low Fertilization Rate, Repeated Pregnancy Loss, Psychological Issues in Infertility, and Animal Biotechnology among many other related topics. The main topics of the 13th Congress on Stem Cell Biology include Cell Technology, Regenerative Medicine, Tissue Engineeringand Cancer Stem Cellsamong others.

This years edition of the congress received 194 papers, 91 of which penned by foreign researchers from US, UK, China, Australia, India, Italy, Lebanon, the Netherlands, Canada, France, Egypt, Belgium, Malaysia, Turkey and Iraq.

MS/4069209

More:
Royan to hold intl. twin congress on reproduction, stem cells - Mehr News Agency - English Version

A*STAR scientists in the Developmental Epigenetics and Disease group. Credit: A*STAR Institute of Molecular and Cell Biology

Embryos kickstart a vibrant genetic program to thrive, but if the wrong genes are active the cells can self-destruct. A*STAR scientists have discovered one of the genes that needs to be tightly locked down for an embryo to develop: a finding that could improve IVF success rates.

Human egg and sperm cells have their genes trained on a single purpose to fertilize. Once their mission is complete, the developing embryo begins the complicated genetic program that turns a single cell into a healthy fetus.

This program is possible thanks in part to epigenetic changes to the DNA, such as the removal of methyl group 'locks' by enzymes, which allows many more genes to be read.

Some specialized genes however need to be locked down during development, as their genetic messages cause problems for the embryo.

"Everything that goes wrong in embryos has the potential to cause infertility or early pregnancy abortions," explains Daniel Messerschmidt from the A*STAR Institute of Molecular and Cell Biology. "We are keen to discover the genomic locations which impact on that development."

Messerschmidt's team previously discovered that a protein called Trim28 locks methyl groups to certain regions in the genome. Now, the researchers looked for the targets of Trim28 to find what genes lies within these regions.

The scientists sequenced the RNA of more than 30 embryos lacking Trim28 and discovered that a gene called Rbmy1a1 was unusually active.

"It's an interesting gene which is not expressed anywhere in the body during development except for spermatogonia in the testes it has no place to be expressed in the embryo," says Messerschmidt. He proposes that the enzyme encoded by Rbmy1a1 produces mRNA transcripts which are harmful to the developing embryo.

Messerschmidt's team is now looking for more of these 'special attention' genes. If the activity of detrimental genes such as Rbmy1a1 can be detected before an embryo is implanted, then it could improve rates of IVF success, says Messerschmidt.

"We want to find out whether we can do epigenetic diagnostics in the same way as when we screen for a suspected genetic disease," he says. "Ultimately, having an overall understanding of these processes will give us a basis for what to look at."

Messerschmidt adds that an epigenetic diagnostic tool for embryos may allow doctors to compare IVF methods which differ between labs. "If we can compare different methods, perhaps we can point doctors to techniques that improve efficiency," he says.

Explore further: Single-cell analysis shows how embryonic cells maintain proper patterns of gene regulation

More information: Abhishek Sampath Kumar et al. Loss of maternalTrim28causes male-predominant early embryonic lethality, Genes & Development (2017). DOI: 10.1101/gad.291195.116

More:
Lockdown genes to reduce IVF failure rates - Medical Xpress

T

he roots of hair loss run deep: Its linked to hormonal balance, immune response, stem cell signaling, and now, according to new research from University of California, Los Angeles metabolism.

The study, published inNature Cell Biology, finds that the metabolism in the stem cells embedded in hair follicles is different from surrounding cells. When they tinkered with that metabolic pathway in mice, they could either halt hair growth or make it proliferate. The UCLA researchers are now testing out a duo of drugs to try and prompt that hair to grow.

This is a STAT Plus article and is only available to STAT Plus subscribers.To read the full story, subscribe to STAT Plus or log in to your account.Good news: your first 30 days are on us.

Biotech Correspondent

Meghana covers biotech and writes The Readout newsletter.

See the original post here:
A new clue to hair loss: A misbehaving enzyme in follicle stem cells - STAT