Monthly Archives: January 2015

Bethesda, MD - The 2015 FASEB Science Research Conference on Genetic Recombination and Genome Rearrangements is an important scientific conference that presents progress in research on diverse aspects of genetic recombination, a critical process that maintains integrity of the genome and that ensures the faithful transmission of the genome between generations. The underlying theme of the 2015 conference will be to foster exchange of information and technology between researchers working on the biochemical, molecular, genetic and cell biological aspects of recombination. This conference provides a unique venue for discussion of recent advances in the study of recombination mechanisms and of their impact on genome integrity. It will foster collaboration between researchers worldwide who are interested in the basic, clinical, and technological relevance of recombination.

FASEB has announced a total of 34 Science Research Conferences (SRC) in 2015. Registration opens January 20, 2015. For more information about an SRC, view preliminary programs, or find a listing of all our 2015 SRCs, please visit http://www.faseb.org/SRC.

Since 1982, FASEB SRC has offered a continuing series of inter-disciplinary exchanges that are recognized as a valuable complement to the highly successful society meetings. Divided into small groups, scientists from around the world meet intimately and without distractions to explore new approaches to those research areas undergoing rapid scientific changes. In efforts to expand the SRC series, potential organizers are encouraged to contact SRC staff at SRC@faseb.org. Proposal guidelines can be found at http://www.faseb.org/SRC.

FASEB is composed of 27 societies with more than 120,000 members, making it the largest coalition of biomedical research associations in the United States. Our mission is to advance health and welfare by promoting progress and education in biological and biomedical sciences through service to our member societies and collaborative advocacy.

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Federation of American Societies for Experimental Biology 9650 Rockville Pike, Bethesda, MD 20814-3998 http://www.faseb.org/SRC-Gene

Contact: Robin Crawford, CMP Office of Scientific Meetings & Conferences 301-634-7010 src@faseb.org

GENETIC RECOMBINATION AND GENOME REARRANGEMENTS Date: July 19-24, 2015, Steamboat Springs, CO Organizers: Michael Lichten, Tanya Paull

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FASEB Science Research Conference: Genetic Recombination and Genome Rearrangements

Spencer Katz

In 2011, researchers announced that they had reprogrammed the genome of the bacteria E. coli, changing it so that one of DNA's methods of encoding information went unused. While a technological tour-de-force, the scientists didn't actually do anything with the newly available bit of genetic code. Now a few years later, two different groups have used it to accomplish the same end: creating genetically modified organisms that may never be able to escape into the wild.

All forms of life we're aware of use what's called a triplet code: it takes three bases in a row in order to encode for one of the amino acids that make up a protein. A series of triplets, stretched out along the DNA, can be read to determine the precise order of amino acids. At the end of the list of amino acid codes, you'll find what's called a stop codon. The three stop codons (TAA, TAG, and TGA in their DNA form) don't code for any amino acids, which the cell interprets as an indication to terminate translation of codes into amino acids.

Since there are three stop codons that mean essentially the same thing, the earlier work involved replacing all instances of one of them (TAG) with a different one (TAA). The editing process preceded in stages but, by the time it was done, all 314 cases where TAG was used as a stop codon had been replaced. This, in effect, freed up TAG to encode something else, such as an artificial amino acid.

While that sounds simple, there are a lot of things that need to be put into place before cells can start using an artificial amino acid (which may explain why these new papers are arriving over three years after the initial work). You have to either find a way to get the cells to make the artificial amino acid, or to import it from the environment. Then, you have to modify an enzyme so that the artificial amino acid gets linked to a key intermediary in protein manufacturing called a transfer RNA.

Both teams (one based at Yale, the other a Boston/Seattle collaboration) take the same approach to getting the amino acid inside a cell: they chose a large, hydrophobic molecule that can easily cross through the hydrophobic membranes that keep other molecules on the outside. They then introduced a new transfer RNA, as well as an enzyme to link the artificial amino acid to it. With that, everything was in place to get the artificial addition working as part of E. coli's genetic code.

To reach their overall goalmaking sure that the bacteria couldn't survive outside the labthey then had to ensure that E. coli needed this amino acid in order to survive. So, both teams obtained a list of essential proteins for which we know the full, three-dimensional structure. They then had computers search these structures for places that the artificial amino acid would fit. Once identified, the teams started going back and editing their new TAG codon into these essential genes, ensuring that they couldn't be made without the artificial amino acid.

To an extent, this worked when just a single essential gene was modified. The bacteria grew well when they were fed the artificial amino acid, and growth quickly ground to a halt when it was taken away. But evolution is a powerful force, and about one in 106 cells would pick up a mutation that allowed it to grow further.

Some of these were mutations elsewhere in the essential protein that allowed them to tolerate amino acids that didn't fit well. Others altered a different transfer RNA so that it replaced the one for the artificial amino acid. Still others got rid of an enzyme that normally chews up defective looking proteins. Bit by bit, the teams eliminated these potential escape routes. They also added to the number of essential genes that were modified to use the artificial amino acid.

By the time they were done, it was impossible to identify a singe bacterium that could escape its reliance on the artificial amino acid. That would mean that, even in a population of over 1012 cells, not one carries a combination of mutations that could allow them to live outside the lab conditions.

Read more here:
Genome engineering used to create a bacterial kill switch

IMAGE:A study conducted in C. elegans worms (left) revealed genes involved in forming long-term memories. These genes are activated by a transcription factor called CREB in the worm's AIM neurons... view more

Credit: Image source: Murphy lab

A new study has identified genes involved in long-term memory in the worm as part of research aimed at finding ways to retain cognitive abilities during aging.

The study, which was published in the journal Neuron, identified more than 750 genes involved in long-term memory, including many that had not been found previously and that could serve as targets for future research, said senior author Coleen Murphy, an associate professor of molecular biology and the Lewis-Sigler Institute for Integrative Genomics at Princeton University.

"We want to know, are there ways to extend memory?" Murphy said. "And eventually, we would like to ask, are there compounds that could maintain memory with age?"

The newly pinpointed genes are "turned on" by a molecule known as CREB (cAMP-response element-binding protein), a factor known to be required for long-term memory in many organisms, including worms and mice.

"There is a pretty direct relationship between CREB and long-term memory," Murphy said, "and many organisms lose CREB as they age." By studying the CREB-activated genes involved in long-term memory, the researchers hope to better understand why some organisms lose their long-term memories as they age.

To identify the genes, the researchers first instilled long-term memories in the worms by training them to associate meal-time with a butterscotch smell. Trained worms were able to remember that the butterscotch smell means dinner for about 16 hours, a significant amount of time for the worm.

The researchers then scanned the genomes of both trained worms and non-trained worms, looking for genes turned on by CREB.

The researchers detected 757 CREB-activated genes in the long-term memory-trained worms, and showed that these genes were turned on primarily in worm cells called the AIM interneurons.

Originally posted here:
Genome-wide search reveals new genes involved in long-term memory