New Type of Male Contraceptive? Key Gene Essential for Sperm Development Discovered

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The finding could lead to alternatives to the conventional male contraceptives that rely on disrupting the production of hormones, such as testosterone. These treatments can cause side-effects such as irritability, mood swings and acne.
Research, led by the University of Edinburgh, has shown how a gene -- Katnal1 -- is critical to enable sperm to mature in the testes.
If scientists can regulate the Katnal1 gene in the testes, they could prevent sperm from maturing completely, making them ineffective without changing hormone levels.
The research, which is published in the journal PLoS Genetics, could also help in finding treatments for cases of male infertility when malfunction of the Katnal1 gene hampers sperm development.
Dr Lee Smith, Reader in Genetic Endocrinology at the University of Edinburgh's Centre for Reproductive Health, said: "If we can find a way to target this gene in the testes, we could potentially develop a non-hormonal contraceptive.
"The important thing is that the effects of such a drug would be reversible because Katnal1 only affects sperm cells in the later stages of development, so it would not hinder the early stages of sperm production and the overall ability to produce sperm.
"Although other research is being carried out into non-hormonal male contraceptives, identification of a gene that controls sperm production in the way Katnal1 does is a unique and significant step forward in our understanding of testis biology."
Scientists found that male mice that were modified so they did not have the Katnal1 gene were infertile.
Further investigation showed that this was because the gene was needed to allow the sperm to develop and mature.
The researchers showed that Katnal1 was needed to regulate the scaffolding structures known as microtubules, which form part of the cells that support and provide nutrients to developing sperm.
Breaking down and rebuilding these microtubules enables the sperm cells to move within the testes as they mature. Katnal1 acts as the essential controller of this process.

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http://www.sciencedaily.com/releases/2012/05/120524215249.htm

MU professor awarded $3.4 million grant to research HIV

An MU professor was awarded a $3.4 million five-year grant for his research to stop a genetic mutation that allows HIV to evade potential treatments.
Stefan Sarafianos, associate professor of molecular microbiology and immunology, said he plans to use the funding to develop a chemical inhibitor designed to target the HIV enzyme RNase H. The enzyme allows the HIV virus to grow through DNA replication.
The RNase H project is a different approach and a totally new target, Sarafianos said.
Sarafianos, who has studied the virus since 1993, is working with University of Pittsburg virologist Michael Parniak and University of Minnesota medicinal chemist Zhengqiang Wang on the project.
Sarafianos is working on mapping the structure of RNase H, while Wang is designing the chemical compound of the inhibitor, and Parniak is evaluating how the compounds interact with the structure.
"A number of people have looked at RNase H and have been unsuccessful," said Tony Conley, the National Institute of Allergy and Infectious Diseases liaison for the project. "Dr. Sarafianos' specialty is in structural biology. He has very good skills and talents to define structure and develop inhibitors.”
NIAID, a branch of the National Institute of Health, awarded the grant. The NIH is made up of 27 institutes and centers each with a separate research agenda, according to the NIH website.
Grant applications from the NIH go through a two-step peer review process to assess scientific merit, according to the NIH website. Two groups of non-federal scientists with relevant research interests and expertise must both recommend the application before funding can be awarded.
The NIH institutes and centers make decisions about funding based on research priorities, according to the NIH website. The NIAID considers funding HIV research a top priority and currently funds hundreds of active research projects, Conley said.
"It would be nice if we knew more about RNase so we could inhibit it," Conley said.
Sarafianos began studying HIV in 1993 because there were a lot of unanswered questions and challenges concerning the virus, he said.
"Twenty years later — my gosh, there is still so much to do,” Sarafianos said.
In 2010 he discovered the N348I mutation, which causes the HIV to resist treatment.
HIV research has led to the development of inhibitors for three other HIV enzymes, Conley said.
Sarafianos worked with Parniak to develop the EFda drug, an extremely potent inhibitor of HIV reverse transcriptase that prevents the virus from copying itself. This drug is undergoing clinical trials.
Sarafianos said he never gets bored of HIV research.
"It's an enigma wrapped in a riddle," Sarafianos said.

Link: http://www.themaneater.com/stories/2013/3/5/mu-professor-awarded-34-million-grant-research-hiv/

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