Science identified the gene for pain

Science has found the gene for pain

Science has found the gene for pain

Scientists have identified a gene essential to the ability to sense pain, a discovery which could be a potential target in the development of new pain relief medications.

The researchers also say there are people who have a mutant copy of the gene and are unable to feel pain from birth.

These people can’t distinguish between unpleasant heat or cold but their other senses, including touch, remain intact.

The study, of people with the rare condition Congenital insensitivity to pain (CIP), is published in the journal Nature Genetics.

The target of new research, to help develop treatments for chronic pain, will be the protein produced by the pain gene.

 

Source:  businessinsider.com.au

500-Million-Year-Old Gene Resurrected

Scientists Place 500-Million-Year-Old Gene in Modern Organism:

Scientists Place 500-Million-Year-Old Gene in Modern Organism

Scientists Place 500-Million-Year-Old Gene in Modern Organism

It’s a project 500 million years in the making. Only this time, instead of playing on a movie screen in Jurassic Park, it’s happening in a lab at the Georgia Institute of Technology.

 

Using a process called paleo-experimental evolution, Georgia Tech researchers have resurrected a 500-million-year-old gene from bacteria and inserted it into modern-day Escherichia coli (E. coli) bacteria. This bacterium has now been growing for more than 1,000 generations, giving the scientists a front row seat to observe evolution in action.

“This is as close as we can get to rewinding and replaying the molecular tape of life,” said scientist Betül Kaçar, a NASA astrobiology postdoctoral fellow in Georgia Tech’s NASA Center for Ribosomal Origins and Evolution. “The ability to observe an ancient gene in a modern organism as it evolves within a modern cell allows us to see whether the evolutionary trajectory once taken will repeat itself or whether a life will adapt following a different path.”

In 2008, Kaçar’s postdoctoral advisor, Associate Professor of Biology Eric Gaucher, successfully determined the ancient genetic sequence of Elongation Factor-Tu (EF-Tu), an essential protein in E. coli. EFs are one of the most abundant proteins in bacteria, found in all known cellular life and required for bacteria to survive. That vital role made it a perfect protein for the scientists to answer questions about evolution.

After achieving the difficult task of placing the ancient gene in the correct chromosomal order and position in place of the modern gene within E. coli, Kaçar produced eight identical bacterial strains and allowed “ancient life” to re-evolve. This chimeric bacteria composed of both modern and ancient genes survived, but grew about two times slower than its counterpart composed of only modern genes.

“The altered organism wasn’t as healthy or fit as its modern-day version, at least initially,” said Gaucher, “and this created a perfect scenario that would allow the altered organism to adapt and become more fit as it accumulated mutations with each passing day.”

The growth rate eventually increased and, after the first 500 generations, the scientists sequenced the genomes of all eight lineages to determine how the bacteria adapted. Not only did the fitness levels increase to nearly modern-day levels, but also some of the altered lineages actually became healthier than their modern counterpart.

When the researchers looked closer, they noticed that every EF-Tu gene did not accumulate mutations. Instead, the modern proteins that interact with the ancient EF-Tu inside of the bacteria had mutated and these mutations were responsible for the rapid adaptation that increased the bacteria’s fitness. In short, the ancient gene has not yet mutated to become more similar to its modern form, but rather, the bacteria found a new evolutionary trajectory to adapt.

The results were presented at the recent NASA International Astrobiology Science Conference. The scientists will continue to study new generations, waiting to see if the protein will follow its historical path or whether it will adopt via a novel path altogether.

“We think that this process will allow us to address several longstanding questions in evolutionary and molecular biology,” said Kaçar. “Among them, we want to know if an organism’s history limits its future and if evolution always leads to a single, defined point or whether evolution has multiple solutions to a given problem.”

Why homosexuality occurs

Study finds epigenetics, not genetics, underlies homosexuality:

Study finds epigenetics, not genetics, underlies homosexuality

Study finds epigenetics, not genetics, underlies homosexuality

 

KNOXVILLE – Epigenetics – how gene expression is regulated by temporary switches, called epi-marks – appears to be a critical and overlooked factor contributing to the long-standing puzzle of why homosexuality occurs. According to the study, published online today in The Quarterly Review of Biology, sex-specific epi-marks, which normally do not pass between generations and are thus “erased,” can lead to homosexuality when they escape erasure and are transmitted from father to daughter or mother to son. From an evolutionary standpoint, homosexuality is a trait that would not be expected to develop and persist in the face of Darwinian natural selection. Homosexuality is nevertheless common for men and women in most cultures. Previous studies have shown that homosexuality runs in families, leading most researchers to presume a genetic underpinning of sexual preference. However, no major gene for homosexuality has been found despite numerous studies searching for a genetic connection. In the current study, researchers from the Working Group on Intragenomic Conflict at the National Institute for Mathematical and Biological Synthesis (NIMBioS) integrated evolutionary theory with recent advances in the molecular regulation of gene expression and androgen-dependent sexual development to produce a biological and mathematical model that delineates the role of epigenetics in homosexuality. Epi-marks constitute an extra layer of information attached to our genes’ backbones that regulates their expression. While genes hold the instructions, epi-marks direct how those instructions are carried out – when, where and how much a gene is expressed during development. Epi-marks are usually produced anew each generation, but recent evidence demonstrates that they sometimes carryover between generations and thus can contribute to similarity among relatives, resembling the effect of shared genes. Sex-specific epi-marks produced in early fetal development protect each sex from the substantial natural variation in testosterone that occurs during later fetal development. Sex-specific epi-marks stop girl fetuses from being masculinized when they experience atypically high testosterone, and vice versa for boy fetuses. Different epi-marks protect different sex-specific traits from being masculinized or feminized – some affect the genitals, others sexual identity, and yet others affect sexual partner preference. However, when these epi-marks are transmitted across generations from fathers to daughters or mothers to sons, they may cause reversed effects, such as the feminization of some traits in sons, such as sexual preference, and similarly a partial masculinization of daughters. The study solves the evolutionary riddle of homosexuality, finding that “sexually antagonistic” epi-marks, which normally protect parents from natural variation in sex hormone levels during fetal development, sometimes carryover across generations and cause homosexuality in opposite-sex offspring. The mathematical modeling demonstrates that genes coding for these epi-marks can easily spread in the population because they always increase the fitness of the parent but only rarely escape erasure and reduce fitness in offspring.”Transmission of sexually antagonistic epi-marks between generations is the most plausible evolutionary mechanism of the phenomenon of human homosexuality,” said the study’s co-author Sergey Gavrilets, NIMBioS’ associate director for scientific activities and a professor at the University of Tennessee-Knoxville.

###

The paper’s other authors are William Rice, a professor at the University of California, Santa Barbara, and Urban Friberg, a professor at Uppsala University in Sweden. The National Institute for Mathematical and Biological Synthesis (NIMBioS) brings together researchers from around the world to collaborate across disciplinary boundaries to investigate solutions to basic and applied problems in the life sciences. NIMBioS is sponsored by the National Science Foundation, the U.S. Department of Homeland Security, and the U.S. Department of Agriculture with additional support from The University of Tennessee, Knoxville. Homosexuality as a consequence of epigenetically canalized sexual development.