Sentences with phrase «elegans by»

Matyash, V., Entchev, E., Mende, F., Wilsch - Bräuninger, M., Thiele, C., Schmidt, A., Knölker, H. - J., Ward, S., and Kurzchalia T. V. Sterol - derived hormone (s) control entry into diapause in Caenorabditis elegans by consecutive activation of DAF - 12 and DAF - 16.

Paralysis and killing of Caenorhabditis elegans by enteropathogenic Escherichia coli requires the bacterial tryptophanase gene.

A study of the development of the nervous system of the nematode Caenorhabditis elegans by Neda Masoudi, Oliver Hobert and colleagues reveals a novel function for a member of the basic helix - loop - helix family of transcription factors in controlling terminal neuron differentiation (rather than initial commitment to a neural fate).

Not exact matches

POISONED BY MOM A C. elegans nematode that inherits a gene for the antidote to a maternal toxin grows a normal feeding tube (shown first).

Led by graduate student Patrick O'Hern, the team at Brown and the University of Cologne in Germany uncovered a complex cause - and - effect sequence in both C. elegans worm and mouse models of SMA.

Data published by the International Human Genome Sequencing Consortium indicate that somewhere between 113 and 223 genes present in bacteria and in the human genome are absent in well - studied organisms — such as the yeast Saccharomyces cerevisiae, the fruit fly Drosophila melanogaster and the nematode Caenorhabditis elegans — that lie in between those two evolutionary extremes.

The researchers discovered that by exposing C. elegans to chemicals that are excreted by P. pacificus, they could elicit a fear - like response.

Researchers studying the nematode worm C. elegans have discovered a new mechanism by which the millimeter - long critter flexes its pooping muscles.

Members of OIST's Information Processing Biology Unit, led by Prof. Ichiro Maruyama, have recently uncovered the sensor for alkaline environments, or high pH, in C. elegans.

For example, it might be possible to create C. elegans worms that protect fields of crops from disease by seeking out harmful bacteria.

Using the model organism, Caenorhabditis elegans, the researchers identified over 400 new mRNA editing sites — the majority regulated by ADR - 1 — and declared the protein the first global regulator of RNA editing.

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.

A quirk of the physiology of C. elegans means that such gene inactivation can occur simply if the RNAi molecule is eaten by the worm.

«By identifying this major regulator of noncoding editing in C. elegans we can now focus on dissecting the regulatory mechanism and determining the conservation of this regulatory protein in human cells.»

Key aspects of ischemia - reperfusion can be modeled by a Caenorhabditis elegans behavior, the O2 - ON response, which is suppressed by hypoxic preconditioning or inactivation of the O2 - sensing HIF (hypoxia - inducible factor) hydroxylase EGL - 9.

The Caenorhabditis elegans Bcl - 2 — like protein CED - 9 prevents programmed cell death by antagonizing the Apaf - 1 — like cell - death activator CED - 4.

«We can explain a lot of the disagreement in the C. elegans aging field by realizing that FuDR can dramatically change the answer,» Hart said.

Curran and his colleagues tweaked the amount of Maf1 in C. elegans, a transparent worm often used as a model organism by biologists.

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.

Tatar's research, along with simultaneous independent work by Linda Partridge of University College London, U.K., and her colleagues, demonstrated that an insulin - like signaling pathway controls diapause and aging in flies — similar to what had already been found in the roundworm Caenorhabiditis elegans (see «Growing Old Together»).

«Calcium dynamics regulating the timing of decision - making in C. elegans: A tiny worm makes a decision by calculating mathematical integration.»

By the turn of the century, the humble nematode worm (Caenorhabditis elegans) will have a rather big claim to fame: all being well, it will be the first animal to have the DNA of its genome, all 100 million base pairs of it, spelt out in full.

Ambros first heard about the bag of worms at a 1979 lecture by Robert Horvitz, who had studied C. elegans in Brenner's Cambridge lab.

«And what this paper confirms in a theoretical model is that you don't need lots of neurons to perform these searches that include switching from a local to a global search — you can approximate it by using just three neurons, as in the roundworm C. elegans.»

In a recent paper in the journal Trends in Ecology and Evolution, Shapira, who studies the gut microbes of the nematode C. elegans, reviews evidence that demonstrates how microbiotas affect and contribute to host evolution, either by evolving along with the host, or by stepping in at critical moments to help the host adapt to a new environmental challenge.

«Scientists have learned a lot about development, gene regulation, and cancer biology, among other things, by studying C. elegans.

In the new study, Lee and his colleagues studied piRNAs produced by cells in the reproductive system of the nematode worm, C. elegans, a classic model organism studied by scientists to understand basic biological processes.

In an experiment led by Leopoldo Sancho from the Complutense University of Madrid, two species of lichen — Rhizocarpon geographicum and Xanthoria elegans — were sealed in a capsule and launched on a Russian Soyuz rocket on 31 May 2005.

C. elegans is a hermaphrodite, and can therefore reproduce by self - fertilization.

(b) An optical image showing a mid-L4 stage C. elegans trapped by multiple oscillating microbubbles.

We prepared transgenic C. elegans lines expressing human PLIN1, PLIN2 and PLIN3 fused to GFP and regulated by the W01A8.1 promoter.

What they found was that when they overexpress transcription factors that drive the specification of specific subtypes of neurons in other cells in C. elegans, these do not by themselves cause the cell to convert into neurons.

Rudolph Tanzi and Robert Moir, who study neurodegeneration at Harvard MGH, sought to test whether amyloid - β might protect mice, Caenorhabditis elegans nematodes, and human cells in culture from invasion by various microbes.

Our results indicate that C. elegans can compensate for the loss of W01A8.1 in all developmental stages except early embryos likely by additional fat degradation mechanisms.

The characteristic aggregation of lipid - containing structures around the embryonic nuclei clearly detected in C. elegans embryos by CARS microscopy are reminiscent of lipid droplets recently reported to be a characteristic feature of cancer stem cells in colorectal carcinomas (Tirinato et al., 2015).

Arantes - Oliveira N, Apfeld J, Dillin A, Kenyon C. Regulation of Lifespan by germ - line stem - cells in Caenorhabditis elegans.

Here we identify the protein encoded by the W01A8.1 gene in Caenorhabditis elegans as the closest homologue and likely orthologue of metazoan perilipin.

His lab is interested in the regulation of gene expression by mRNA processing in C. elegans and human cells.

Surprisingly, in laboratory conditions C. elegans can overcome the complete loss of the perilipin - related protein W01A8.1, presumably by activating perilipin - independent lipid degradation.

The protein encoded by W01A8.1 in C. elegans is identified as Mediator Complex subunit 28 (MDT - 28) in many protein databases (e.g., Pfam, UniProt, PIR, WormPep)(accessed on March 14, 2015), but the bioinformatics analysis reveals that this is a misannotation.

Steffen Jaensch (Hyman, MPG)-- «Time - resolved quantification of centrosomes by automated image analysis suggests limiting component to set centrosome size in C. elegans embryos» (2010)

Symmetry breaking and polarization of the C. elegans zygote by the polarity protein PAR - 2.

Dr. Hansen's group focused on investigating the molecular mechanisms by which the nutrient sensor TOR modulates aging, using the nematode C. elegans as her primary model organism.

Activation of SKN - 1 by novel kinases in Caenorhabditis elegans.

Learning about the recent discovery of C. elegans» so - called «sister species» — Species 34 — by Gavin Woodruff in Okinawa.

Researchers have discovered the molecular mechanisms by which the roundworm C. elegans senses oxygen concentrations in the highly variable soil environment where it lives.

Researchers have discovered that a new neurotransmitter — a chemical message sent by neurons — exists in the roundworm C. elegans.

In yeast and Caenorhabditis elegans, the majority of ORFs revealed by genomic sequencing have not been associated with mutant phenotypes, even in genomic regions that have been subjected to saturation mutagenesis (36 - 37).

Analysis of RNA - protein complexes by RNA coimmunoprecipitation and RT - PCR analysis from Caenorhabditis elegans.

Analysis of in vivo protein complexes by coimmunoprecipitation from Caenorhabditis elegans.