Category Archives: Transhuman News

One kind of stem cell, those referred to as 'facultative', form part -- together with other cells -- of tissues and organs. There is apparently nothing that differentiates these cells from the others. However, they have a very special characteristic, namely they retain the capacity to become stem cells again. This phenomenon is something that happens in the liver, an organ that hosts cells that stimulate tissue growth, thus allowing the regeneration of the organ in the case of a transplant. Knowledge of the underlying mechanism that allows these cells to retain this capacity is a key issue in regenerative medicine.

Headed by Jordi Casanova, research professor at the Instituto de Biologa Molecular de Barcelona (IBMB) of the CSIC and at IRB Barcelona, and by Xavier Franch-Marro, CSIC tenured scientist at the Instituto de Biologa Evolutiva (CSIC-UPF), a study published in the journal Cell Reports reveals a mechanism that could explain this capacity. Working with larval tracheal cells of Drosophila melanogaster, these authors report that the key feature of these cells is that they have not entered the endocycle, a modified cell cycle through which a cell reproduces its genome several times without dividing.

"The function of endocycle in living organisms is not fully understood," comments Xavier Franch-Marro. "One of the theories is that endoreplication contributes to enlarge the cell and confers the production of high amounts of protein." This is the case of almost all larval cells of Drosophila.

The scientists have observed that the cells that enter the endocycle lose the capacity to reactivate as stem cells. "The endocycle is linked to an irreversible change of gene expression in the cell," explains Jordi Casanova, "We have seen that inhibition of endocycle entry confers the cells the capacity to reactivate as stem cells."

Cell entry into the endocycle is associated with the expression of the Fzr gene. The researchers have found that inhibition of this gene prevents this entry, which in turn leads to the conversion of the cell into an adult progenitor that retains the capacity to reactivate as a stem cell. Therefore, this gene acts as a switch that determines whether a cell will enter mitosis (the normal division of a cell) or the endocycle, the latter triggering a totally different genetic program with a distinct outcome regarding the capacity of a cell to reactivate as a stem cell.

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The above story is based on materials provided by Institute for Research in Biomedicine (IRB Barcelona). Note: Materials may be edited for content and length.

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Mechanism that allows differentiated cell to reactivate as a stem cell revealed

PUBLIC RELEASE DATE:

29-Oct-2014

Contact: Krista Conger kristac@stanford.edu 650-725-5371 Stanford University Medical Center @sumedicine

The ability to pop a working copy of a faulty gene into a patient's genome is a tantalizing goal for many clinicians treating genetic diseases. Now, researchers at the Stanford University School of Medicine have devised a new way to carry out this genetic sleight of hand.

The approach differs from that of other hailed techniques because it doesn't require the co-delivery of an enzyme called an endonuclease to clip the recipient's DNA at specific locations. It also doesn't rely on the co-insertion of genetic "on" switches called promoters to activate the new gene's expression.

These differences may make the new approach both safer and longer-lasting. Using the technique, the Stanford researchers were able to cure mice with hemophilia by inserting a gene for a clotting factor missing in the animals.

"It appears that we may be able to achieve lifelong expression of the inserted gene, which is particularly important when treating genetic diseases like hemophilia and severe combined immunodeficiency," said Mark Kay, MD, PhD, professor of pediatrics and of genetics. "We're able to do this without using promoters or nucleases, which significantly reduces the chances of cancers that can result if the new gene inserts itself at random places in the genome."

Using the technique, Kay and his colleagues were able to insert a working copy of a missing blood-clotting factor into the DNA of mice with hemophilia. Although the insertion was accomplished in only about 1 percent of liver cells, those cells made enough of the missing clotting factor to ameliorate the disorder.

Kay is the senior author of the research, which will be published Oct. 29 in Nature. The lead author is postdoctoral scholar Adi Barzel, PhD.

A possible alternative to CRISPR

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New way of genome editing cures hemophilia in mice; may be safer than older method

For his contribution to the understanding of gene regulation and its potential ability to change agriculture and the treatment of disease and mental health, Professor Ryan Lister has been awarded the 2014 Frank Fenner Prize for Life Scientist of the Year.

Genes are not enough to explain the difference between a skin cell and a stem cell, a leaf cell and a root cell, or the complexity of the human brain. Genes dont explain the subtle ways in which your parents environment before you were conceived might affect your offspring.

Another layer of complexitythe epigenomeis at work determining when and where genes are turned on and off.

Ryan Lister is unravelling this complexity. Hes created ways of mapping the millions of molecular markers of where genes have been switched on or off, has made the first maps of these markers in plants and humans, and revealed key differences between the markers in cells with different fates.

Hes created maps of the epigenome in plants, which could enable plant breeders to modify crops to increase yields without changing the underlying DNA.

Hes explained a challenge for stem cell medicineshowing how, when we persuade, for example, skin cells to turn into stem cells, these cells retain a memory of their past. Their epigenome is different to that of natural embryonic stem cells. He believes this molecular memory could be reversed.

He has also recently explored the most complex system we knowthe human braindiscovering that its epigenome is extensively reconfigured in childhood during critical stages when the neural circuits are forming and maturing. These epigenome patterns may even underpin learning and memory. All of this in just 15 years since the beginning of his PhD.

For his contribution to the understanding of gene regulation and its potential ability to change agriculture and the treatment of disease and mental health, Professor Ryan Lister of the Australian Research Council Centre of Excellence in Plant Energy Biology at the University of Western Australia has been awarded the 2014 Frank Fenner Prize for Life Scientist of the Year.

The human body is composed of hundreds of different types of cells. Yet all are formed from the same set of instructions, the human genome. How does this happen?

On top of the genetic code sits another code, the epigenome. It can direct which genes are switched on and which are switched off, Ryan Lister says. The genome contains a huge volume of information, a parts list to build an entire organism. But controlling when and where the different components are used is crucial. The epigenetic code regulates the release of the genomes potential. Cells end up with different forms and functions through using different parts of the genome.

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Regulating genes to treat illness, grow food, and understand the brain