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Next-gen organoids grow and function like real tissues — ScienceDaily

Organoids are fast-becoming one of the most cutting-edge tools of modern life sciences. The idea is to use stem cells to build miniature tissues and organs that accurately resemble and behave like their real counterparts.

One can immediately appreciate the value of organoids for both research and medicine: from basic biological research to drug development and testing, organoids could complement animal testing by providing healthy or diseased human tissues, expediting the lengthy journey from lab to clinical trial. Beyond that, there is already the whisper of organoid technology perhaps being used for replacing damaged tissues or even organs in the future: take stems cells from the patient and grow them into a new liver, heart, kidney, or lung.

So far, established methods of making organoids come with considerable drawbacks: stem cells develop uncontrollably into circular and closed tissues that have a short lifespan, as well as non-physiological size and shape, all of which result in overall anatomical and/or physiological inconsistency with real-life organs.

Now, scientists from the group led by Matthias Lütolf at EPFL’s Institute of Bioengineering have found a way to “guide” stem cells to form an intestinal organoid that looks and functions just like a real tissue. Published in Nature, the method exploits the ability of stem cells to grow and organize themselves along a tube-shaped scaffold that mimics the surface of the native tissue, placed inside a microfluidic chip (a chip with little channels in which small amounts of fluids can be precisely manipulated).

The EPFL researchers used a laser to sculpt this gut-shaped scaffold within a hydrogel, a soft mix of crosslinked proteins found in the gut’s extracellular matrix supporting the cells in the native tissue. Aside from being the substrate on which the stem cells could grow, the hydrogel thus also provides the form or “geometry” that would build the final intestinal tissue.

Once seeded in the gut-like scaffold, within hours, the stem cells spread across the scaffold, forming a continuous layer of cells with its characteristic crypt structures and villus-like domains. Then came the surprise: the scientists found that, the stem cells just “knew” how to arrange themselves in order to form a functional tiny gut.

“It looks like the geometry of the hydrogel scaffold, with its crypt-shaped cavities, directly influences the behavior of the stem cells so that they are maintained in the cavities and differentiate in the areas outside, just like in the native tissue,” says Lütolf. The stem cells didn’t just adopt to the shape of the scaffold, they produced all the key differentiated cell types found in the real gut, with some rare and specialized cell types normally not found in organoids.

Intestinal tissues are known for the highest cell turnover rates in the body, resulting in a massive amount of shed dead cells accumulating in the lumen of the classical organoids that grow as closed spheres and require weekly breaking down into small fragments to maintain them in culture. “The introduction of a microfluidic system allowed us to efficiently perfuse these mini-guts and establish a long-lived homeostatic organoid system in which cell birth and death are balanced,” says Mike Nikolaev, the first author of the paper.

The researchers demonstrate that these miniature intestines share many functional features with their in vivo counterparts. For example, they can regenerate after massive tissue damage and they can be used to model inflammatory processes or host-microbe interactions in a way not previously possible with any other tissue model grown in the laboratory.

In addition, this approach is broadly applicable for the growth of miniature tissues from stem cells derived from other organs such as the lung, liver or pancreas, and from biopsies of human patients. “Our work shows that tissue engineering can be used to control organoid development and build next-gen organoids with high physiological relevance, opening up exciting perspectives for disease modelling, drug discovery, diagnostics and regenerative medicine,” says Lütolf.

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Materials provided by Ecole Polytechnique Fédérale de Lausanne. Original written by Nik Papageorgiou. Note: Content may be edited for style and length.

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A new discovery in regenerative medicine — ScienceDaily

An international collaboration involving Monash University and Duke-NUS researchers have made an unexpected world-first stem cell discovery that may lead to new treatments for placenta complications during pregnancy.

While it is widely known that adult skin cells can be reprogrammed into cells similar to human embryonic stem cells that can then be used to develop tissue from human organs — known as induced pluripotent stem cells (iPSCs) — the same process could not create placenta tissue.

iPSCs opened up the potential for personalised cell therapies and new opportunities for regenerative medicine, safe drug testing and toxicity assessments, however little was known about exactly how they were made.

An international team led by ARC Future Fellow Professor Jose Polo from Monash University’s Biomedicine Discovery Institute and the Australian Research Medicine Institute, together with Assistant Professor Owen Rackham from Duke-NUS in Singapore, examined the molecular changes the adult skin cells went through to become iPSCs. It was during the study of this process that they discovered a new way to create induced trophoblast stem cells (iTSCs) that can be used to make placenta cells.

This exciting discovery, also involving the expertise of three first authors, Dr. Xiaodong Liu, Dr. John Ouyang and Dr. Fernando Rossello, will enable further research into new treatments for placenta complications and the measurement of drug toxicity to placenta cells, which has implications during pregnancy.

“This is really important because iPSCs cannot give rise to placenta, thus all the advances in disease modelling and cell therapy that iPSCs have brought about did not translate to the placenta,” Professor Polo said.

“When I started my PhD five years ago our goal was to understand the nuts and bolts of how iPSCs are made, however along the way we also discovered how to make iTSCs,” said Dr Liu.

“This discovery will provide the capacity to model human placenta in vitro and enable a pathway to future cell therapies,” commented Dr Ouyang.

“This study demonstrates how by successfully combining both cutting edge experimental and computational tools, basic science leads to unexpected discoveries that can be transformative,” Professor Rackham said.

Professors Polo and Rackham said many other groups from Australian and international universities contributed to the study over the years, making it a truly international endeavour.

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Materials provided by Monash University. Note: Content may be edited for style and length.

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Scientists are learning about species adaptation by comparing their stem cell-related genes — ScienceDaily

The genes regulating pluripotent stem cells in mammals are surprisingly similar across 48 species, Kyoto University researchers report in the journal Genome Biology and Evolution. The study also shows that differences among these ‘gene regulating networks’ might explain how certain features of mammalian pluripotent stem cells have evolved.

Pluripotent stem cells can self-renew and give rise to all other types of cells in the body. Their characteristics are controlled by a network of regulatory genes and molecules, but little is known about how this network has evolved across mammals.

To this end, Ken-ichiro Kamei of Kyoto University’s Institute for Integrated Cell-Material Sciences (iCeMS), with Miho Murayama and Yoshinori Endo of the Wildlife Research Center, compared 134 gene sets belonging to the pluripotency gene regulatory networks of 48 mammalian species.

They found that this network has been highly conserved across species, meaning genetic sequences have remained relatively unchanged over the course of evolution. This high degree of conservation explains why human genetic sequences can reprogram other mammalian tissue cells to turn into pluripotent stem cells. However, since it is also evident that the regulating networks differ across mammals, there might be more efficient combinations of reprogramming factors for each species. Improving techniques for deriving induced pluripotent stem (iPS) cells from mammalian cells, including those from endangered species, could provide a big boost to research and conservation.

“We have been trying to generate induced pluripotent stem cells from various mammalian species, such as the endangered Grévy’s zebra and the bottlenose dolphin,” says Kamei.

Interestingly, the team found relatively high evolutionary changes in genes just downstream of one of the core gene regulatory networks. “This could indicate that mammalian pluripotent stem cells have diversified more than we thought,” says Inoue-Murayama.

The differences between gene regulatory networks in mammalian pluripotent stem cells might also be associated with unique adaptions.

For example, the naked mole rat has been positively selected for a pluripotency regulatory gene that could be involved in giving it its extraordinary longevity and cancer resistance. The gene might also be involved in the development of the extremely sensitive hairs that help them navigate underground.

The researchers also found evidence of positive selection for certain pluripotency gene regulatory network genes involved in the adaptation of large animals, such as the minke whale, the African elephant and the flying fox, to their environments. Surprisingly, these same genes are associated with cancer in other mammals. Since these large animals are known for being relatively resistant to cancer, the researchers suggest that the adaptive alterations these genes underwent in these animals somehow also changed some of their functions, thus giving this group a degree of cancer resistance.

The researchers say the study is among the first to compare the pluripotency gene regulatory networks across major taxa, and could be applicable to evolutional biology studies and for facilitating and improving the generation of induced pluripotent stem cells from new species.

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Materials provided by Kyoto University. Note: Content may be edited for style and length.

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Gene that drives ovarian cancer identified — ScienceDaily

High-grade serious ovarian carcinoma (HGSOC) is the fifth-leading cause of cancer-related deaths in women in the United States, yet little is known about the origins of this disease.

Now, scientists at the College of Veterinary Medicine have collaborated on a study that pinpoints which specific genes drive — or delay — this deadly cancer.

“We’ve taken the enormous collection of genomic mutation data that’s been mined on cancer genetics and tried to make functional sense of it,” said John Schimenti, professor of genetics in the Department of Biomedical Sciences and senior author of the study, which published Sept. 1 in Cell Reports.

Schimenti teamed with biomedical sciences colleague Alexander Nikitin, professor of pathology and director of the Cornell Stem Cell Program, and members of their respective labs to gain a better understanding of HGSOC.

Cancer researchers have known for a while that the disease is almost always caused by multiple genetic “hits.” One mutation alone does not turn a cell cancerous; generally at least two or three are required, and often different combinations of genes can cause the same cancer.

Adding complexity, Schimenti said, is the fact that once one key genome-destabilizing mutation arises, others will follow. Sequenced tumors yield a plethora of mutations — some are the originators of the cancer itself, while many others are spinoffs.

“It’s a longstanding issue in cancer research,” he said. “What are the genetic drivers, and what are the passengers in the process?”

To address these complexities, the researchers wanted to test combinations of possible genetic suspects, and then parse out which of the many associated mutations were sparking the cancer.

To do so, they turned to the Cancer Genome Atlas, an international collaborative database that compiles the genetic information from patient tumor samples and the mutated genes associated with them. They took a list of 20 genes known to mutate in HGSOC and, using CRISPR gene-editing technology, created random combinations of these mutations in cultured cells from the ovary surface, including regular epithelial cells and epithelial stem cells, to see which cell type was more susceptible to the mutations.

The researchers then noted which combination of mutations turned which group of cells cancerous — pinpointing both the genes driving the process and which cell type the cancer originated in.

The study revealed what the team had originally suspected — that ovarian surface stem cells were more apt to become cancerous when hit with mutations. They also unexpectedly discovered genes that had the opposite effect.

“We found there were various genes that would help the process along, but interestingly, there were other genes that, when mutated, actually inhibited the cancer initiation process,” Schimenti said.

Knowing which are the cells of origin and which genes are necessary in initiating this highly aggressive form of ovarian cancer can be powerful information, both for ovarian and other types of cancers. “The cancer driver screening methodology we used should be applicable to answering the same kinds of questions for cells and cancers in other organs and tissues,” Nikitin said.

Schimenti said the findings could be particularly useful for ovarian cancer patients who have their tumors biopsied and sequenced for genetic data.

“In the past, you would know which genes were mutated but you wouldn’t know what role they played,” he said. “Now you know which ones are important. And eventually, you could develop drugs to target the mutated genes that you know are causing the problem.”

This work was supported by grants from the Ovarian Cancer Research Fund, the New York State Stem Cell Science Program, the National Institutes of Health and the National Cancer Institute.

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Materials provided by Cornell University. Original written by Lauren Cahoon Roberts. Note: Content may be edited for style and length.

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Mini-organs could offer treatment hope for children with intestinal failure — ScienceDaily

Pioneering scientists at the Francis Crick Institute, Great Ormond Street Hospital (GOSH) and UCL Great Ormond Street Institute of Child Health (ICH) have grown human intestinal grafts using stem cells from patient tissue that could one day lead to personalised transplants for children with intestinal failure, according to a study published in Nature Medicine today (Monday 7th September).

Children with intestinal failure cannot absorb the nutrients that are essential for their overall health and development. This may be due to a disease or injury to their small intestine.

In these cases, children can be fed intravenously via a process called parenteral nutrition, however this is associated with severe complications such as line infections and liver failure. If complications arise or in severe cases these children may need a transplant. However, there is a shortage of suitable donor organs and problems can arise after surgery, such as the body rejecting the transplant.

In their proof-of-concept study, the research team showed how intestinal stem cells and small intestinal or colonic tissue taken from patients can be used to grow the important inner layer of small intestine in the laboratory with the capacity to digest and absorb peptides and digest sucrose in food.

This is the first step in efforts to engineer all the layers of the intestine for transplantation. The researchers hope that one day, laboratory grown organs could offer a safe and longer-lasting alternative to traditional donor transplants.

“It’s urgent that we find new ways to care for children without a working intestine because, as they grow older, complications from parental nutrition can arise,” says Dr Vivian Li, senior author and group leader of the Stem Cell and Cancer Biology Laboratory at the Crick.

“We’ve set out a process to grow one layer of intestine in the laboratory, moving us a step closer to being able to offer these patients a form of regenerative medicine, which uses materials created from their own tissue. This would reduce some of the risks that transplant patients face, such as their immune system attacking the transplant.”

The researchers took small biopsies of intestine from 12 children who either had intestinal failure or were at risk of developing the condition. In the lab, they then stimulated the biopsy cells to grow into “mini-guts,” also known as intestinal organoids, generating over 10 million intestinal stem cells from each patient over the course of 4 weeks.

The researchers also collected small intestine and colon tissue, that would otherwise have been discarded, from other children undergoing essential surgery to remove parts of their gut. Using laboratory techniques, cells were removed from these tissues leaving behind a skeleton structure which formed scaffolds.

The researchers placed the “mini-guts” onto these scaffolds, where they grew on this structure to form a living graft. Due to specific culture conditions, the stem cells changed into many of the different types of cells that exist in the small intestine. The grafts were able to digest and absorb peptides, the building blocks of proteins, as well as digest sucrose into glucose sugars.

“Although this research is in the lab right now, we’re concentrating on making this a realistic and safe treatment option,” explains senior author NIHR Professor Paolo De Coppi, Consultant Paediatric Surgeon at GOSH and Head of Surgery, Stem Cells & Regenerative Medicine Section at the UCL Great Ormond Street Institute of Child Health (ICH).

“What’s significant here is we’ve shown that scaffolds can be created using tissue from the colon, not only tissue from the small intestine. In practice, it is often easier to obtain tissue from the colon, so this could make the approach much more feasible. It’s an important step forward in regenerative medicine and we’re optimistic about what this means for patients, but more research lies ahead before we can safely and effectively translate this approach to treatment.”

As well as proving that biopsies taken from children could be used to grow functioning intestinal grafts, the researchers also demonstrated that the grafts survive and mature when transplanted into mice.

“By applying our basic science knowledge of intestinal stem cell biology, we have developed a time efficient and clinically relevant method for rebuilding human small intestine grafts for transplantation,” says Laween Meran, lead author, Gastroenterology Registrar and Clinical Research Training Fellow at the Stem Cell and Cancer Biology Laboratory at the Crick and the ICH.

“Now that we’ve shown the grafts are successful on a small scale, the next crucial steps will be to start growing the other layers of the intestine such as muscle and blood vessels, whilst also scaling up our methods to create viable grafts relevant to individual patient needs.”

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New gel deposition technique — ScienceDaily

Researchers at the University of Illinois Chicago have developed a unique method for precisely controlling the deposition of hydrogel, which is made of water-soluble polymers commonly used to support cells in experiments or for therapeutic purposes. Hydrogel mimics the extracellular matrix — the natural environment of cells in the body.

The researchers noticed that their technique — which allows for the encapsulation of a single cell within a minute hydrogel droplet — can be used to coax bone marrow stem cells into specialized cells.

Their findings are reported in the journal Advanced Science.

The new technique is an improvement over existing approaches that often mix much larger amounts of hydrogel with cells in an uncontrolled manner, which can make interactions between cells and their surroundings difficult to study. The new hydrogel deposition technique may also be useful for therapeutic purposes, such as for supporting stem cells used to create new tissues.

“Most experiments use a very high amount of hydrogels to interface with cells, which may not reflect what is happening in the body,” said UIC’s Jae-Won Shin, assistant professor of pharmacology and regenerative medicine at the College of Medicine, and assistant professor of bioengineering at the College of Engineering, and corresponding author on the paper.

According to Shin, the team’s deposition technique brings the ratio between hydrogels and cells in-line with what is seen in the body, and importantly, precisely controls the ratio on a single cell basis.

Shin and colleagues also observed that stem cells in thinner gel droplets expanded more rapidly than they did in bulk gels.

“We observed that stem cells expand several orders of magnitude faster in thin gel droplets, and so they experience more tension than they do in bulk gels made of the same material,” said Sing Wan Wong, a postdoctoral fellow in Shin’s lab and first author on the study. “We believe this tension encourages stem cells in thin gel coatings to more readily become bone cells, compared to stem cells in bulk gels.”

The team believes the thin hydrogel deposition technique may help in the production of bone tissue from stem cells to use as regenerative therapeutics.

Stephen Lenzini, Raymond Bargi, Celine Macaraniag, James C. Lee and Zhangli Peng of UIC and Zhe Feng of the University of Notre Dame are co-authors on the paper.

This research was supported by grants from the National Institutes of Health (R01HL141255, R00HL125884) and the National Science Foundation (1948347-CBET).

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Materials provided by University of Illinois at Chicago. Note: Content may be edited for style and length.

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Breakthrough in using stem cells to treat enteric nervous system disorders — ScienceDaily

Scientists have made a breakthrough in understanding how the enteric nervous system forms, which could pave the way for new treatments for neurodegenerative diseases such as Parkinson’s.

The findings, published in the journal Stem Cell Reports, pave the way for using stem cells to understand and treat a range of diseases linked to the enteric nervous system — which is embedded in the walls of the esophagus, stomach, small and large intestines, pancreas, gallbladder and biliary tree.

Researchers from the University of Sheffield and University College London (UCL) identified a key stage in the formation of the enteric nervous system using pluripotent stem cells, which can generate any cell type in the body, and were able to generate enteric neurons in the lab.

The enteric nervous system contains between 400-600 million nerves and is crucial for everyday functions such as digestion, fluid absorption and communicating with the immune system.

Faults in the enteric nervous system are often linked to life-threatening digestive disorders such as Hirschprung’s disease, where nerves in the system are missing. Ongoing research has also suggested that Parkinson’s disease is initiated in the enteric nervous system before reaching the brain.

Dr Anestis Tsakiridis,Group Leader of the Study from the University of Sheffield’s Centre for Stem Cell Biology, said: “Our findings show new promise for using stem cells to treat a range of diseases. We now plan to utilise these findings as the basis for developing stem cell-based approaches to treat and model diseases caused by dysfunction of the enteric nervous system.”

Dr Tom Frith, from the Francis Crick Institute who led the study said: “This work was the result of an exciting collaboration with experts from the UCL Great Ormond Street Institute of Child Health.

“These results are a key first step into generating cells in a dish that may one day be used to help treat patients.”

The team involved in the study have been awarded a £1.2 million grant from the Medical Research Council (MRC), which focuses on the development of a stem cell therapy for the treatment of Hirschprung’s disease.

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Materials provided by University of Sheffield. Note: Content may be edited for style and length.

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Researchers pinpoint hierarchy of breast cancer cells as potential cause for treatment resistance — ScienceDaily

University of Cincinnati instructor Syn Yeo, PhD, thinks the same analogy applies when it comes to cells and the growth of cancer, particularly breast cancer.

In his recent study, published in the journal eLife, Yeo, research instructor in the department of cancer biology at the UC College of Medicine and co-lead author, says it can take cells in different forms or “life stages” to cause cancer to grow and spread.

“Our recent findings emphasize the need to account for the specific cell states that are present within a tumor,” says Yeo, who is a member in the lab of Jun-Lin Guan, PhD, the Francis Brunning Endowed Chair and professor of cancer biology. “This could potentially help determine the combination of drugs that are required to eliminate all the cell states that are present to eliminate treatment resistance.”

Yeo says that when it comes to breast cancers, it is known that cells within a tumor are varied.

“This diversity poses a problem to treating patients because particular subsets of tumor cells may be drug resistant and eventually lead to disease recurrence,” he says. “One of the factors contributing to this diversity is the fact that tumor cells can exist in different cellular states, ranging from more stem-like cells that can become other cell types to more differentiated cells that have been coded to serve a purpose, or do a certain ‘job’ within the system.

“Cancer cells with stem-like properties are known to cause drug resistance, and they are generally seen as being at the top of the tumor hierarchy, like the kKing or queen of the village, with more differentiated tumor cells towards the bottom of the hierarchy, like the common townspeople.”

In this study, researchers used breast cancer animal models to determine tumor hierarchies beyond “ruler” and “common people” cells, Yeo says. They identified and categorized singular cells which helped them understand each, individual cell’s purpose. Yeo adds that bulk tumor cell analysis would have masked the cellular details.

“We were able to find a complex spectrum of cell states between different tumor types that can range from stem-cells to the ‘beginner cells’ to more differentiated cells,” he says. “In our village [scenario], these would be the governors and mayors, followed by the common townspeople. Furthermore, depending on the lineage of the tumor, some may show a spectrum of cell states that are higher up in the hierarchy and vice versa.

“These findings are important because they show we need to know more about how these specific cell states contribute to tumor growth so we can target them with combination drug therapies, potentially helping more people who may otherwise experience drug resistance.”

Funding for this research was provided by the National Institutes of Health (R01-CA211066, R01-HL073394 and R01-NS094144). Xiaoting Zhu was the other co-lead author who was partially supported by R01-HL111829. Other contributors include Takako Okamoto, Mingang Hao, Cailian Wang, Peixin Lu, Long Jason Lu and Jun-Lin Guan. Researchers cite no conflict of interest.

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Materials provided by University of Cincinnati. Original written by Katie Pence. Note: Content may be edited for style and length.

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A new molecular guardian of intestinal stem cells — ScienceDaily

Intestinal stem cells keep a fine balance between two potential forms: remaining as stem cells, or developing into intestinal epithelial cells. In a new study, researchers from Tokyo Medical and Dental University (TMDU) discovered a novel molecular mechanism that regulates this balance and preserves the stemness of intestinal stem cells — that is, their ability to develop into any intestinal epithelial cell type.

The inner lining of intestines, the intestinal epithelium, ensures adequate digestion and adsorption of nutrients. It is made up of several different cell types, all of which fulfill a specific function. Intestinal stem cells ensure proper functioning of the intestines, which requires constantly replacing old and damaged cells with young cells, by developing, or differentiating, into one of the different intestinal epithelial cell types when needed. Because there is a constant demand for new cells, intestinal stem cells have the ability to self-renew, thereby providing a constant supply of stem cells as well. However, little is known about the mechanisms that regulate this balance between self-renewal and differentiation.

“Just like any other type of stem cell, intestinal stem cells have the ability to differentiate into any cell within their lineage,” says corresponding author of the study Professor Toshiaki Ohteki. “But they have to do it in a regulated manner, only differentiating when needed. The goal of our study was to understand the regulatory mechanism that preserves the stemness of intestinal stem cells.”

To achieve their goal, Taku Sato, a main contributor of this project, and collaborators focused on a molecular signaling pathway that they had previously shown to preserve the stemness of hematopoietic stem cells (HSCs) that give rise to blood cells. Interferons are molecules that are produced especially during viral and bacterial infections, but more recently it was also shown that they are present even in the absence of infections to regulate various biological processes. In either case, interferons induce the expression of certain genes, a process that is regulated by the protein interferon regulatory factor-2 (IRF2) to ensure that the actions of interferons are balanced. In the case of HSCs, IRF2 turned out to be a critical factor for their stemness.

In the current study, the researchers found that IRF2 is produced throughout the intestinal epithelium and that IRF2-deficient mice had normal anatomical structure during homeostasis (the absence of an infection or any other damaging factor). However, in the presence of 5-fluorouracil, which is known to damage the intestinal epithelium, normal mice were able to regenerate completely, but IRF2-deficient mice showed a blunted regenerative response indicating that intestinal stem cells were not able to function properly in the absence of IRF2. Interestingly, immature Paneth cells, which are specialized secretory cells, were highly abundant in IRF2-deficient mice. The researchers had the same finding in normal mice exposed to lymphocytic choriomeningitis virus (LCMV), which causes chronic infection.

“These are striking results that show how excess interferon signaling in the absence of IRF2 impairs the ability to self-renew and directs intestinal stem cells towards the secretory cell lineage. Our findings provide new insight into the biology of intestinal stem cells and show that regulated interferon signaling is a means to preserve the stemness of intestinal stem cells,” says Professor Ohteki.

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Materials provided by Tokyo Medical and Dental University. Note: Content may be edited for style and length.

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Becoming a nerve cell: Timing is of the essence

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Researchers find that mitochondria regulate a key event during brain development: how neural stem cells become nerve cells. Mitochondria influence this cell fate switch during a precise period that is twice as long in humans compared to mice. This highlights an unexpected function for mitochondria that may help explain how humans developed a bigger brain during evolution, and how mitochondrial defects lead to neurodevelopmental diseases.

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