Sentences with phrase «elegans genes»

Based on similarity to C. briggsae, we found strong evidence for 1,300 new C. elegans genes.

Since the early 1990s, researchers have linked mutations in dozens of C. elegans genes to extension of the creature's life.

Tissue taken from mice with the C. elegans gene had significantly higher levels of omega - 3 acids compared with that of normal animals, the team found.

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).

Biologists have for decades discussed how two genes in the familiar lab nematode Caenorhabditis elegans might help embryos build their organs.

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.

But to my mind that is not how it has turned out — rather the reverse with a near equivalence of a modest 20,000 genes across the vast range of organismic complexity from the millimetre - long Caenorhabditis elegans to the 60 - trillion - celled Homo sapiens.

These results showed that different genes control the life span of C. elegans and the length of reproductive time.

Already, researchers have used CRISPR / Cas9 to edit genes in human cells grown in lab dishes, monkeys (SN: 3/8/14, p. 7), dogs (SN: 11/28/15, p. 16), mice and pigs (SN: 11/14/15, p. 6), yeast, fruit flies, the worm Caenorhabditis elegans, zebrafish, tobacco and rice.

To answer this question, Murphy tracked which genes were turned on and off over time in the oocytes and somatic cells in C. elegans IGF - 1 and TGF - β mutants, as well as wild - type worms.

When Murphy compared the genes turned off and on in oocytes and body cells of the same worm, however, she saw that two completely different sets of genes controlled oocyte and body - cell aging in C. elegans.

Murphy found that the normal pattern of gene activation seen in aging wild - type C. elegans was reversed in the body cells and oocytes of IGF - 1 mutants.

Strome noted that the findings in this study of transmission of histone methylation in C. elegans have important implications in other organisms, even though different organisms use the repressive marker that was studied to regulate different genes during different aspects of development.

But it turns out that we have only about 25,000 genes — about the same number as a tiny flowering plant called Arabidopsis and barely more than the worm Caenorhabditis elegans.

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.

Both studies relied on a popular lab organism known as C. elegans, a nearly microscopic nematode that is fast growing, translucent and has a sequenced genome showing that nearly half its genes are closely related to corresponding human genes.

After bombarding hundreds of Caenorhabditis elegans worms with DNA - altering chemicals and screening the results, he found that the deletion of just one gene rendered the worms almost completely resistant to alcohol.

Yet when scientists refined it last spring, the count had dropped to little more than 30,000, only a third more genes than a simple worm like Caenorhabditis elegans.

«C. elegans is a powerful tool for biological research because it shares many of the same anatomic and cell functions as humans, and their short lifespan (average 17 days) enables us to study genes and measure cell traits in just two to three weeks.»

Two projects will be done jointly with the Karolinska Institute in Stockholm: Molecular biologist David Baillie of Simon Fraser University in Burnaby, British Columbia, was awarded $ 6.73 million to study protein function in the soil nematode Caenorhabditis elegans, and microbiologist Sherif Abou Elela of the University of Sherbrooke, Quebec, received $ 3.75 million to test modified nucleic acid technologies for determining gene function.

They were studying how a worm called C. elegans would react when different genes were deleted from its DNA.

When he failed, he devoted his attention to other genes involved in the development of C. elegans.

CK: We have studies in C. elegans showing that the daf - 2 gene functions exclusively in the adult to control aging.

One of the mutants carries a defect in Sch9, which resembles two genes in the C. elegans daf - 2 pathway.

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

Meanwhile, Esvelt and his colleagues are studying the CRISPR gene - drive system in the nematode Caenorhabditis elegans to learn more about what happens to a population as engineered DNA is passed down through generations, accumulating mutations as it goes.

Dubbed model - organism ENCODE (modENCODE), this new focus will apply innovative methods and technologies for the study of gene regulation to the smaller, and therefore more manageable, genomes of the fruit fly (Drosophila melanogaster) and the round worm (Caenorhabditis elegans).

In old C. elegans specimens, those treated with dietary restrictions (right) showed more youthful gene splicing patterns than naturally - aged animals (left)(Credit: Caroline Heintz)

This unusual evolutionary gap in the perilipins prompted us to re-examine the C. elegans genome for a gene related to mammalian perilipin.

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.

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.

In old C. elegans specimens, those treated with dietary restrictions (right) showed more youthful gene splicing patterns than naturally - aged animals (left)(Credit: Caroline Heintz)

Human perilipins 1 and 2 localize in transgenic C. elegans on the same structures as proteins expressed from W01A8.1 gene.

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.

Publication T. Wilhelm et al., Neuronal inhibition of the autophagy nucleation complex extends life span in post-reproductive C. elegans, Genes & Development, 7 September 2017, DOI: 10.1101 / gad.301648.117

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.

Not content to provide just the missing evidence for a 60 - year - old puzzle, Wilhelm and his colleagues went on to describe what a subset of these genes do in C. elegans and how they might be driving the ageing process.

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

We used RNA - mediated interference to target 98 % of all genes predicted in the C. elegans genome in combination with differential interference contrast time - lapse microscopy.

Most of the study's experiments were done in the roundworm C. elegans, which have an SMN gene and motor neurons — those that connect to muscle — that are very similar to humans, making them valuable models in which to study this disease.

«There's a large degree of conservation between the genes that are affecting regeneration efficiency in planarians and genes in C. elegans, Drosophila and humans,» says S ‡ nchez Alvarado.

«SapTrap, a Toolkit for High - Throughput CRISPR / Cas9 Gene Modification in Caenorhabditis elegans.»

By deliberately introducing defined sequences of dsRNA into living organisms, biologists can observe the physiological consequences of «silencing» virtually any gene in C. elegans, as well as other plants and animals.

Despite its power, RNAi is amazingly simple to perform in the roundworm C. elegans, an important model system for eukaryotic gene function.

An adult C. elegans with GFP coding sequence inserted into a histone - encoding gene.

Professor Bargmann then embarked upon what was to become a lifetime mission to define how genes and the environment influence behavior by dissecting the neural circuitry of C. elegans and the genes, receptors, and signaling molecules involved in such behavior as feeding and responses to odors.

These broad associations with complexity are evidently superimposed on notable lineage - specific variation as seen in Fig. 4 (for example, serine protease gene loss in C. elegans, and voltage-gated ion channel expansion in Paramecium).

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.