Are you looking for read ebook online? Search for your book and save it on your Kindle device, PC, phones or tablets. Download Viable Maternal Effect Mutations In The Nematode Caenorhabditis Elegans PDF full book. Access full book title Viable Maternal Effect Mutations In The Nematode Caenorhabditis Elegans.
| Author | : Paula Boutis |
| Publisher | : |
| Total Pages | : 114 |
| Release | : 1995 |
| Genre | : Animal mutation |
| ISBN | : |
| Author | : Claire Y. H. Bénard |
| Publisher | : |
| Total Pages | : 348 |
| Release | : 2003 |
| Genre | : Caenorhabditis elegans |
| ISBN | : |
"Le role des contributions epigenetiques lors du developpement d'un zygote en un organisme adulte a ete etudie a travers la caracterisation genetique et moleculaire de deux genes a effet maternel, mau-2 et clk-2, chez le nematode C. elegans. Des mutations dans ces deux genes produisent des patrons d'heritabilite differents, ainsi que des phenotypes distincts. Les mutants mau-2 sont secourus partiellement par un effet maternel, mais sont normaux quand un allele de type sauvage est exprime chez le zygote. Le gene mau-2 participe au guidage de nombreuses migrations de cellules et axones lors du developpement. Ce gene code pour une proteine de fonction inconnue, qui a ete conservee lors de l'evolution. mau-2 fonctionne dans les cellules qui migrent pendant le developpement du systeme nerveux. D'autre part, les mutants clk-2 sont completement secourus maternellement, excepte pour leurs competences reproductrices. De plus, ils dependent strictement de la presence d'un allele de type sauvage chez la mere pour leur developpement embryonnaire. clk-2 est requis pour la regulation des rythmes du developpement et du comportement. clk-2 est un gene essentiel, dont la fonction est requise entre la fin de la maturation des oocytes et le stade embryonnaire de deux cellules. clk-2 code pour une proteine qui est similaire a Tel2p, une proteine chez la levure, et est requis pour le maintien d'une longeur normale des telomeres chez le ver. Bien que mau-2 et clk-2 fonctionne differemment pendant le developpement du ver, la base de l'effet maternel semble etre tres similaire dans les deux cas. Une quantite considerable de transcrit est accumule dans les oocytes et est probablement transferee au zygote. Le transcrit ainsi fourni au zygote permet la traduction de proteine de type sauvage en quantite suffisante pour mener la plupart des fonctions de ces deux genes lors du developpement." --
| Author | : Yan Meng |
| Publisher | : |
| Total Pages | : 194 |
| Release | : 2000 |
| Genre | : Caenorhabditis elegans |
| ISBN | : |
"In an effort to find new genes involved in development and the biological timing, I carried out a new screen for viable maternal-effect mutations similar in protocol to the previous screen in which 24 such genes have been identified. I screened 10,600 genomes and isolated 6 slow-growing mutations and 5 behavioral and morphological mutations. Another maternal-effect slow-growing mutation is isolated from a screen for both maternal-effect and non maternal-effect slow development mutations. Genetic mapping suggests that none of the seven slow growing mutations corresponds to previously identified genes, so seven new clk genes (clk-4, clk-5, clk-6, clk-7 clk-8, clk-9, clk-10) have been identified. Because most identified clk genes (clk-2, clk-4 to clk-10 and gro-1) are defined by single allele, we believe that these genes have not yet been saturated. Mutants of seven new clk genes have typical Clk phenotypes: a mean lengthening of embryonic development, postembryonic development, defecation cycle and life span. As the screening procedure did not involve any measure of life span, it is suggested that slow life is sufficient for long life. As expected, all seven mutations can be maternally rescued." --
| Author | : Joseph Veyhl |
| Publisher | : |
| Total Pages | : |
| Release | : 2013 |
| Genre | : |
| ISBN | : |
| Author | : Amy Kristin Adams |
| Publisher | : |
| Total Pages | : 102 |
| Release | : 1995 |
| Genre | : |
| ISBN | : |
| Author | : Jason Burgess |
| Publisher | : |
| Total Pages | : 190 |
| Release | : 2002 |
| Genre | : Caenorhabditis elegans |
| ISBN | : |
"Mutations in the Caenorhabditis elegans maternal-effect gene clk-1 result in a highly pleiotropic phenotype, characterized by a general slow down in embryonic and larval development, as well as a slowing down of adult behaviors including defecation, pharyngeal pumping and swimming. First generation homozygous clk-1 mutants descended from a heterozygous mother are fully rescued for these mutant phenotypes. It has been shown that CLK-1 protein is a hydroxylase that acts in the conversion of demethoxyubiquinone (DMQ) to 5-hydroxyubiquinone, in the ubiquinone (Q) biosynthesis pathway. Consequently, clk-1 mutants accumulate the Q9 precursor, DMQ9 (the subscript refers to the length of the isoprenoid side chain). Here, I show that the profound maternal rescue observed in clk-1 maternally rescued animals is due to presence of the CLK-1 protein throughout larval development, in sufficient amounts to catalyze the production of Q9. clk-1 mutants have been shown to have a dietary requirement for Q8 due to their inability to synthesize Q9. I demonstrate that clk-1 maternally rescued animals have sufficient amounts of Q 9 to complete larval development and produce an almost full brood when raised on a Q8 deficient E. coli strain. I also show that prolonged arrest at the first larval stage, which is likely to result in degradation of any maternally contributed mRNA or protein, brings about a Clk mutant phenotype in maternally rescued animals. Finally, I reveal that the Clk mutant phenotype can be rescued at any larval stage by ectopic expression of CLK-1, suggesting that there is no developmental window for the rescue of clk-1 mutants by CLK-1. These results identify perdurance of maternally contributed product throughout development as the mechanism that accounts for the maternal effect observed in clk-1 mutants." --
| Author | : Donald L. Riddle |
| Publisher | : Firefly Books |
| Total Pages | : 1252 |
| Release | : 1997 |
| Genre | : Medical |
| ISBN | : 9780879695323 |
Defines the current status of research in the genetics, anatomy, and development of the nematode C. elegans, providing a detailed molecular explanation of how development is regulated and how the nervous system specifies varied aspects of behavior. Contains sections on the genome, development, neural networks and behavior, and life history and evolution. Appendices offer genetic nomenclature, a list of laboratory strain and allele designations, skeleton genetic maps, a list of characterized genes, a table of neurotransmitter assignments for specific neurons, and information on codon usage. Includes bandw photos. For researchers in worm studies, as well as the wider community of researchers in cell and molecular biology. Annotation copyrighted by Book News, Inc., Portland, OR
| Author | : National Research Council |
| Publisher | : National Academies Press |
| Total Pages | : 348 |
| Release | : 2000-12-21 |
| Genre | : Nature |
| ISBN | : 0309070864 |
Scientific Frontiers in Developmental Toxicology and Risk Assessment reviews advances made during the last 10-15 years in fields such as developmental biology, molecular biology, and genetics. It describes a novel approach for how these advances might be used in combination with existing methodologies to further the understanding of mechanisms of developmental toxicity, to improve the assessment of chemicals for their ability to cause developmental toxicity, and to improve risk assessment for developmental defects. For example, based on the recent advances, even the smallest, simplest laboratory animals such as the fruit fly, roundworm, and zebrafish might be able to serve as developmental toxicological models for human biological systems. Use of such organisms might allow for rapid and inexpensive testing of large numbers of chemicals for their potential to cause developmental toxicity; presently, there are little or no developmental toxicity data available for the majority of natural and manufactured chemicals in use. This new approach to developmental toxicology and risk assessment will require simultaneous research on several fronts by experts from multiple scientific disciplines, including developmental toxicologists, developmental biologists, geneticists, epidemiologists, and biostatisticians.
| Author | : Siegfried Hekimi |
| Publisher | : Springer Science & Business Media |
| Total Pages | : 254 |
| Release | : 2012-12-06 |
| Genre | : Science |
| ISBN | : 354048003X |
The molecular genetics of aging or life-span determination is an expanding field. One reason is because many people would consider it desirable if hu man life span could be extended. Indeed, it is difficult not to be fascinated by tales of the life and death of people who have succeeded in living a very long life. Because of this, we have placed at the head of this book the chapter by Perls et al. on Centenerians and the Genetics of Longevity. Perls and his coauthors convincingly argue that, while the average life expectancy might be mostly determined by environmental factors because the average person has an average genotype, extremely long life spans are genetically determined. Of course, studying humans to uncover the genetics of aging is not ideal, not so much because one cannot easily perform experiments as because they live such a long time. This is why most of this book describes the current state of research with model organisms such as yeast, worms, flies, and mice. J aswinski focuses on yeast and how metabolic activity and stress resistance affect the longevity of Saccharomyces cerevisiae. In the process, he discusses the concept of aging as applied to a unicellular organism such as yeast and the importance of metabolism and stress resistance for aging in all organisms.
| Author | : M.P. Mattson |
| Publisher | : Elsevier |
| Total Pages | : 227 |
| Release | : 2003-12-01 |
| Genre | : Science |
| ISBN | : 0080494765 |
Experts in the fields of energy metabolism, aging and oxidative stress provide an integrated view of how mechanisms involved in regulating energy metabolism are linked to fundamental processes of aging including cellular stress resistance and free radical production. During evolution signal transduction pathways and organ systems have been optimised for the efficient seeking, ingestion, storing and using of energy. These signalling pathways play prominent roles in lifespan determination with insulin and related signalling pathways being prime examples. The authors consider how lifespan and healthspan can be extended through knowledge of energy metabolism with the experimental model of dietary restriction being one example. The information in this volume of ACAG will foster novel approaches and experiments for further understanding the roles of energy metabolism in aging and disease.
