Sentences with phrase «elegans genetic»

Two other strains carrying the unc - 124 (hs10) mutation have been deposited with the C. elegans Genetic Center, and we sequenced the unc - 7 region in HH123 unc - 2 (e55) unc - 124 (hs10) and HH132 dpy - 8 (e130) unc - 124 (hs10); the same unc - 7 mutation was identified in both strains.

We conclude that there is no Unc mutation that maps to the left of lin - 2 in unc - 124 (hs10) strains currently held at the C. elegans Genetic Center, and that hs10 is an allele of unc - 7.

Not exact matches

A maternal - effect selfish genetic element in Caenorhabditis elegans.

In a new study, Murphy, a molecular biologist at Princeton University, showed that long - lived bodily, or somatic, cells in Caenorhabditis elegans, a one - millimeter nematode commonly used as a model for aging studies in labs, activate genetic pathways completely separate from those found in long - lived egg, or oocyte, cells.

By comparing our genetic make - up to the genomes of mice, chimps and a menagerie of other species (rats, chickens, dogs, pufferfish, the microscopic worm Caenorhabditis elegans, the fruit fly Drosophila melanogaster and many bacteria), scientists have learned a great deal about how genes evolve over time, and gained insights into human diseases.

In Caenorhabditis elegans, the introduction of double - stranded RNA triggers sequence - specific genetic interference (RNAi) that is transmitted to offspring.

In the classic genetic model Caenorhabditis elegans, the pro-apoptotic protein CED - 4 activates the CED - 3 caspase and is inhibited by the Bcl - 2 — like protein CED - 9.

His group studies the cellular and genetic control of gastrulation movements in zebrafish, one of the model organisms studied at the institute besides Drosophila, the C. elegans worm, frogs, mice, and newts.

With further experimental analysis, the scientists identified two distinct genetic variants that resulted in these sensitivity differences, suggesting that in crowded places, wild C. elegans populations with a specific genetic variation adopt different behaviors than those who don't.

To assess the role of hlh - 1 in C. elegans myogenesis, genetic deficiencies spanning the hlh - 1 locus were isolated after gamma irradiation.

As our role in the HapMap concluded, we took on a new grant: constructing the genetic map of C. briggsae, a small roundworm similar to the well - known model organism, C. elegans.

That year, I joined the lab of Raymond E. Miller, which played a role in the International HapMap Project and later the genetic map of C. briggsae, a model organism related to C. elegans.

With only a single gene and a toolbox of forward and reverse genetic approaches at hand, C. elegans offers an opportunity to explore the exact role of perlipin - related factors in fat regulation throughout development of many different somatic and germline cells.

Moreover, large - scale screens in the C. elegans DMD model allowed identifying genetic and pharmacologic suppressors of dystrophin - dependent muscle degeneration; some of them positively impact mitochondrial functions or structure under stress conditions, or are involved in signaling pathways linked to mitochondria, and others are associated to proteostasis pathways such as autophagy, proteasome and Unfolded Protein Response (UPR).

There, she has established the worm C. elegans as a novel model organism to examine the cellular transformations involved during a direct reprogramming event in vivo, as well as the genetic cascade involved.

In a recent publication in the journal Genes & Development titled «Neuronal inhibition of the autophagy nucleation complex extends lifespan in post-reproductive C. elegans,» Dr. Holger Richly's lab at IMB has found some of the first genetic evidence that may put this question to rest.

To identify novel genes and conserved cellular processes that regulate the biology of K2P channels in vivo we take advantage of the powerful genetic tools available in the model nematode Caenorhabditis elegans.

Her graduate thesis focused on the genetic regulation of innate immunity in C. elegans.

The tiny roundworm C. elegans shares over 40 % of its genetic information with humans and its short lifespan makes it especially well - suited for defining genes that influence healthy lifespan.

Caenorhabditis elegans, a worm with just 302 neurons, shows considerable sophistication in its behaviors, and its defined neuronal wiring and genetic accessibility make it an ideal subject in which to study these interactions.

Genetic and pharmacological analysis of neurotransmitters controlling egg laying in C. elegans.

Dr. Falk is also PI of an NIH, pharma, and philanthropic funded translational research laboratory group at CHOP that investigates the causes and global metabolic consequences of mitochondrial disease, as well as targeted therapies, in C. elegans, zebrafish, mouse, and human tissue models of genetic - based respiratory chain dysfunction, and directs multiple clinical treatment trials in mitochondrial disease patients.

«At first glance there's little similarity between the small roundworm C. elegans and us humans, but at cellular level around 35 % of their genetic makeup is closely related to ours.

Since 2013 Dr. Lithgow has been a leader of the C. elegans Interventions Testing Program, and his presentation highlighted the surprising lack of reproducibility observed between nominally identical lifespan studies — an anomaly that can not be attributed to differences in genetic background or experimental procedure.

For 50 years of brilliant creativity in biomedical science — exemplified by his legendary work on the genetic code; his daring introduction of the roundworm Caenorhabditis elegans as a system for tracing the birth and death of every cell in a living animal; his rational voice in the debate on recombinant DNA; and his trenchant wit.

Jennifer Hammock 在 «Caenorhabditis elegans» 页面将 «File: Environmental - and - Genetic - Preconditioning - for - Long - Term - Anoxia - Responses - Requires - AMPK - in - pone.0016790.

C. elegans is an excellent model for understanding the genetic control of development and physiology.