Female sex determining gene identified in mice

 

Researchers from the Francis Crick Institute and the University Côte d'Azur, in collaboration with labs in France and Switzerland, made a breakthrough by identifying the key role of the Wt1 gene in early ovary development in mice. In mice, the presence of XY or XX chromosomes leads to testes or ovaries development. This outcome is determined by the activity of specific genes including the Sry gene on the Y chromosome (responsible for testes development). The research revealed that the -KTS form of the Wt1 protein is important for the formation of both Sertoli and granulosa cells in gonad development. When the researchers genetically manipulated mice to produce only the -KTS form of the protein, an excess of -KTS inhibited the expression of Sry in XY gonads (which prevents testes development). XY mice with an abundance of -KTS developed female gonads which demonstrated that -KTS is a key early trigger for female gonad development regardless of the chromosome configuration (XX or XY).

In humans mutations in WT1 can lead to Frasier syndrome, which affects kidney function and gonad development. Individuals with XY chromosomes and Frasier syndrome develop ovaries, which degenerate before birth. This discovery not only provides insight into the crucial early stages of gonad development and its impact on an individual's sex determination but also has broader implications for understanding WT1's role in kidney development. Wilms tumor, which is a type of kidney cancer, is also an uncovering mechanism underlying cell fate determination.

Links -

Female sex determining gene identified in mice | ScienceDaily

Researchers identify female sex determining gene in mice (phys.org)

Heterogenous impact on longevity in mice

 

According to the research article "Sex- and age-dependent genetics of longevity in a heterogeneous mouse population" there is no one gene that controls aging and life span but a variety that contribute along with environmental factors. UM-HET3 mice were used by the  National Institute on Aging’s Interventions Testing Program in order to determine the correlation of genes, sex, age, and access to nutrition to longevity. On chromosome 12 a locus was found to have a direct impact on longevity when males and females were analyzed together. However, the females were analyzed separately it was found that a loci on chromosome three contributed to life span. In addition, many factors non genetic factors were confirmed contributors to shortening the life span of the mice like; litter size in females, body weight, and access to nutrients. Boston University's School of Medicine is working on a centenarian study  which agrees with the fact that there are multiple genes that contribute to longevity in humans more specifically. They did find that lifestyle is a large contributing factor for lifespan. They found 281 genes that act as markers and predict the individual will live over a hundred years old. The research that is being done on longevity in humans and other mammals is showing how large of an impact lifestyle has on life span and how genetics due play a role in a longer life span. 

I found both of these articles particularly interesting because of humans obsessions with aging and long life spans. Studies being done on how lifestyle impacts longevity could be very important for the age ranges that are not reaching sexual maturity in order to reproduce to maintain population. More specifically, this is important for individuals who do not live a healthy lifestyle to see how large of an impact it can have on one's life span. 

Mutant ferrets' shine a light on human brain evolution

People are honored with moderately expansive brains. What's more, amid the previous 7 million years; a brief span traverse in trans-formative terms — the measure of our brains has tripled.

The cerebral cortex, the convoluted and collapsed external layer, is especially so in people. Precisely why and how our brains turned out to be so darned extravagant is a state of much level headed discussion and the confirmation is as of now sparse.

Discovering intimations as to hereditary and organic moves that happened a huge number of years back is like searching for a needle in a bundle on the opposite side of the universe. From time to time, be that as it may, Lady Serendipity favors researchers.


As of late, analysts from various establishments, including the Howard Hughes Medical Institute in Chevy Chase, MD, Yale University in New Haven, CT, and Boston Children's Hospital in Massachusetts, directed a progression of concentrates taking a gander at microcephaly.

Their examinations were productive and assist our comprehension of microcephaly, yet they additionally crawled us nearer to that needle in the far off bundle. Their discoveries were as of late distributed in the diary Nature.

Mouse brains are, as you may expect, minor. Likewise, mice despise an indistinguishable different determination of mind cells from people, and their cortex is much smoother.

The quality most usually engaged with microcephaly is one that codes for a protein known as Aspm. At the point when this quality is changed, a human's mind will associate with a large portion of the typical size.

Notwithstanding, in mice without the quality — called Aspm knockout mice — their brains shrivel by only one tenth. This scarcely perceivable change is of little use to researchers.

On the chase for a superior model of microcephaly, the specialists — who were driven by Dr. Walsh and Byoung-Il Bae, from Yale University — swung to ferrets.

Link #1 & Link #2

Possible Gene Manipulation for Diabetes Cure

First lets distinguish the types of diabetes without going into much detail. Type 1 results when the body's immune response destroys the cells responsible for producing insulin these cells are called beta cells. Type 2 occurs when your body can't effectively keep up with the insulin demands of your body.  

With diabetes type 1 and 2 on the rise within the United States and throughout the world, scientists are looking around every corner to find a way to either prevent or cure diabetes. Dr. Francesca and her team from Max Delbruck Center for Molecular Medicine have found a way to reprogram liver cells into pancreatic beta cells in mice. This reprogram process occurs by introducing additional copies of the TGIF2 gene found on chromosome 2 of mice which reprograms the liver cells to take on an unspecialized state and stimulates the development of liver cells into pancreatic beta cells.

Although this study was not done on humans, progress and a new discovery has been made. This research brings genetic therapy for human diabetic patients a step closer for a cure. This is amazing research since so many lives are restricted by this disease. With the continuous study of the TGIF2 gene a cure may be within the near future.

The interesting part of this discovery for me that leaves me with a few questions is with the introduction of an increased amount of a certain gene would this lead to other mutations and to what degree? Would the mutations if any influence the degree to which other genes are expressed?
https://www.sciencedaily.com/releases/2017/02/170213083736.htm
http://www.genecards.org/cgi-bin/carddisp.pl?gene=TGIF2