Author: John Marshall IvyPublisher:
ISBN:
Category : Meiosis
Languages : en
Pages : 222
Book Description
Mutations that Disrupt Meiosis in Males of Drosophila Melanogaster
Author: John Marshall IvyPublisher:
ISBN:
Category : Meiosis
Languages : en
Pages : 222
Book Description
Genetic Variations of Drosophila melanogaster
Author: DAN L. LINDSLEYExploring the Mechanism of Meiosis in Drosophila Melanogaster
Author: Publisher:
ISBN:
Category :
Languages : en
Pages : 201
Book Description
Sister chromatid cohesion is essential for proper chromosome segregation during meiosis. However, the mechanism of meiotic cohesion in Drosophila is unclear. We describe a novel protein, SOLO (Sisters On the LOose) that is essential for meiotic cohesion in Drosophila melanogaster. solo mutations cause high nondisjunction of sister and homologous chromatids of sex chromosomes and autosomes in both sexes. In solo males, sister chromatids separate prematurely and segregate randomly during meiosis II. Although bivalents appear intact throughout meiosis I, sister centromeres lose cohesion prior to prometaphase I and orient nearly randomly on the meiosis I spindle. Centromeric foci of SMC1 are absent in solo males at all meiotic stages. SOLO and the cohesin protein SMC1 co-localize to meiotic centromeres from early prophase I until anaphase II in wild-type males but both proteins are removed prematurely from centromeres at anaphase I in mei-S332 mutants, coincident with premature loss of cohesion in those mutants. solo mutations in females cause reduced frequency of homologous recombination between X chromosomes and autosomes, partially due to the loss of inhibition of sister chromatid exchange. Synaptonemal complex assembly is severely disrupted in early meiotic stage in solo females. SOLO colocalizes with SMC1 and C(3)G in meiosis. Additionally, SOLO is required for stabilizing chiasmata generated from residual recombination events. The data about the phenotypes of solo males and females and colocalization patterns of SOLO strongly suggest SOLO is a component of potential cohesin in Drosophila meiosis. Drosophila males undergo meiosis without recombination. However, the underlying mechanism is not known. Mutations of vasa cause high frequency of X-Y exchange in meiosis. Chromatin bridges at anaphase I and II, due to dicentric recombination events, were observed in vasa males. vas and solo double mutant showed precocious segregation of homologs at metaphase I besides chromatin bridge at anaphase I and II. Our data thus for the first time demonstrate that inhibition of meiotic recombination during male meiosis requires vas function and interactions between vas and solo regulate chromosome dynamics in male meiosis.
THE MUTANTS OF DROSOPHILA MELANOGASTER
Author: CALVIN B. BRIDGESThe Genetics and Manifestations of Certain New Mutations in Drosophila Melanogaster
Author: Emanuel WaletzkyA Meiotic Mutant which Causes a Polarized Disruption of Chromosome Pairing in Female Drosophila Melanogaster
Author: Dilys Myfanwy ParryPublisher:
ISBN:
Category : Drosophila melanogaster
Languages : en
Pages : 202
Book Description
Regulation of Sumoylation by DTopors During Male Meiosis in Drosophila Melanogaster
Author: Avik MukherjeePublisher:
ISBN:
Category : Cancer
Languages : en
Pages : 55
Book Description
"The Topors protein is a tumor suppressor in human that associates with and regulates a number of cell cycle regulators that including topoisomerase I and p53. It possesses both ubiquitin and SUMO ligase activity and its mutation or downregulation has been associated with some human cancers and diseases. The Drosophila homologue, dTopors, is an ubiquitin E3 ligase. We have investigated the role of Dtopors in sumoylating proteins in the male germ line. Although nuclear lamin localization is disrupted in dtopors mutants, we find no evidence of lamin modification by Dtopors. We observe an increase in the overall sumoylation of testis proteins and a corresponding decrease in the pool of free SUMO in homozygous dtopors versus heterozygous dtopors flies. Based on this result, we propose a model explaining the role of dtopors in altering germline sumoylation. We have constructed a SUMO-GFP transgenic protein to investigate how dtopors is altering the pool of SUMO in the cell. We demonstrate that this transgenic construct can rescue smt3 mutant flies and is expressed in spermatocytes. This tool will allow one to measure SUMO synthesis and processing, and how these aspects of SUMO dynamics are affected by dtopors during meiosis in D. melanogaster males."--Abstract from author supplied metadata.
Health Effects of Exposure to Low Levels of Ionizing Radiation
Author: National Research CouncilPublisher: National Academies
ISBN: 0309039959
Category : Science
Languages : en
Pages : 436
Book Description
This book reevaluates the health risks of ionizing radiation in light of data that have become available since the 1980 report on this subject was published. The data include new, much more reliable dose estimates for the A-bomb survivors, the results of an additional 14 years of follow-up of the survivors for cancer mortality, recent results of follow-up studies of persons irradiated for medical purposes, and results of relevant experiments with laboratory animals and cultured cells. It analyzes the data in terms of risk estimates for specific organs in relation to dose and time after exposure, and compares radiation effects between Japanese and Western populations.
Gene Knockout Protocols
Author: Ralf KühnPublisher: Humana Press
ISBN: 9781934115268
Category : Science
Languages : en
Pages : 0
Book Description
Following the completion of the mouse and human genome sequences, a major challengeisthefunctionalcharacterizationofeverymammaliangeneandthedeciph- ing of their molecular interaction network. The mouse offers many advantages for the use of genetics to study human biology and disease, unmatched among other m- mals. Its development, body plan, physiology, behavior, and diseases have much in common, based on the fact that 99% of the human genes have a mouse ortholog. The investigation of gene function using mouse models is based on many years of tech- logical development. In the two decades since gene targeting in murine embryonic stem (ES) cells was first described by Mario Capecchi and colleagues, more than 3000 predesigned mouse mutants have been developed. To date, a variety of mouse mutagenesis techniques, either gene- or phenotype-driven, are used as systematic approaches. The availability of the genome sequence supports gene-driven approaches such as gene-trap and targeted mutagenesis in ES cells, allowing efficient and precise gene disruption. In combination with the use of site-specific DNA recombinases, in particular the Cre/loxP system, gene disruptioncan be directed to specific cell types in conditionalmousemutants. Furthermore,chemicalandtransposonmutagenesisofthe mouse genome enables us to perform phenotype-driven screens for the unbiased identification of phenotype–genotype correlations involved in models of human d- ease. Over the next several years, the mouse genome will be systematically altered, and the techniques for achieving predesigned manipulations will be constantly developed further and improved. The second edition of Gene Knockout Protocols brings together distinguished c- tributorswithextensiveexperienceinthegenetargetingandmousegeneticsfields.
Author: Ben Roy Golden