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971.
Recombinational DNA double-strand breaks in mice precede synapsis 总被引:24,自引:0,他引:24
Mahadevaiah SK Turner JM Baudat F Rogakou EP de Boer P Blanco-Rodríguez J Jasin M Keeney S Bonner WM Burgoyne PS 《Nature genetics》2001,27(3):271-276
In Saccharomyces cerevisiae, meiotic recombination is initiated by Spo11-dependent double-strand breaks (DSBs), a process that precedes homologous synapsis. Here we use an antibody specific for a phosphorylated histone (gamma-H2AX, which marks the sites of DSBs) to investigate the timing, distribution and Spo11-dependence of meiotic DSBs in the mouse. We show that, as in yeast, recombination in the mouse is initiated by Spo11-dependent DSBs that form during leptotene. Loss of gamma-H2AX staining (which in irradiated somatic cells is temporally linked with DSB repair) is temporally and spatially correlated with synapsis, even when this synapsis is 'non-homologous'. 相似文献
972.
973.
Boyartchuk VL Broman KW Mosher RE D'Orazio SE Starnbach MN Dietrich WF 《Nature genetics》2001,27(3):259-260
We have used a novel quantitative trait locus model to study the genetics of survival of F2 progeny of susceptible BALB/cByJ and resistant C57BL/6ByJ mice that have been infected with Listeria monocytogenes. This allowed us to map modifiers of L. monocytogenes susceptibility to chromosomes 5 and 13. 相似文献
974.
DNA double-strand breaks: signaling, repair and the cancer connection 总被引:38,自引:0,他引:38
975.
976.
Targeted deletion of the gene encoding iron regulatory protein-2 causes misregulation of iron metabolism and neurodegenerative disease in mice 总被引:23,自引:0,他引:23
977.
978.
Joyce S 《Cellular and molecular life sciences : CMLS》2001,58(3):442-469
Cellular and humoral immune mechanisms recruited to defend the host from infectious agents depend upon the early immune events
triggered by antigen. The cytokine milieu within which the immune response matures is the most important of many factors that
govern the nature of the immune response. Natural T cells, whose function is controlled by CD1d molecules, are an early source
of cytokines that can bestow type 1 or type 2 differentiative potential upon helper T lymphocytes. This review attempts to
illuminate the glycolipid antigen presentation properties of CD1d, how CD1d controls the function of natural T cells and how
CD1d and natural T cells interact to jump start the immune system. CD1d is postulated to function as a sensor, sensing alterations
in cellular lipid content by virtue of its affinity for such ligands. The presentation of a neo-self glycolipid, presumably
by infectious assault of antigen-presenting cells, activates natural T cells, which promptly release pro-inflammatory and
anti-inflammatory cytokines and jumpstart the immune system.
Received 10 July 2000; received after revision 16 October 2000, accepted 16 November 2000 相似文献
979.
A 5-bp deletion in ELOVL4 is associated with two related forms of autosomal dominant macular dystrophy 总被引:20,自引:0,他引:20
Zhang K Kniazeva M Han M Li W Yu Z Yang Z Li Y Metzker ML Allikmets R Zack DJ Kakuk LE Lagali PS Wong PW MacDonald IM Sieving PA Figueroa DJ Austin CP Gould RJ Ayyagari R Petrukhin K 《Nature genetics》2001,27(1):89-93
Stargardt-like macular dystrophy (STGD3, MIM 600110) and autosomal dominant macular dystrophy (adMD) are inherited forms of macular degeneration characterized by decreased visual acuity, macular atrophy and extensive fundus flecks. Genetic mapping data suggest that mutations in a single gene may be responsible for both conditions, already known to bear clinical resemblance. Here we limit the minimum genetic region for STGD3 and adMD to a 0.6-cM interval by recombination breakpoint mapping and identify a single 5-bp deletion within the protein-coding region of a new retinal photoreceptor-specific gene, ELOVL4, in all affected members of STGD3 and adMD families. Bioinformatic analysis of ELOVL4 revealed that it has homology to a group of yeast proteins that function in the biosynthesis of very long chain fatty acids. Our results are therefore the first to implicate the biosynthesis of fatty acids in the pathogenesis of inherited macular degeneration. 相似文献
980.
Batourina E Gim S Bello N Shy M Clagett-Dame M Srinivas S Costantini F Mendelsohn C 《Nature genetics》2001,27(1):74-78
Mutations or rearrangements in the gene encoding the receptor tyrosine kinase RET result in Hirschsprung disease, cancer and renal malformations. The standard model of renal development involves reciprocal signaling between the ureteric bud epithelium, inducing metanephric mesenchyme to differentiate into nephrons, and metanephric mesenchyme, inducing the ureteric bud to grow and branch. RET and GDNF (a RET ligand) are essential mediators of these epithelial-mesenchymal interactions. Vitamin A deficiency has been associated with widespread embryonic abnormalities, including renal malformations. The vitamin A signal is transduced by nuclear retinoic acid receptors (RARs). We previously showed that two RAR genes, Rara and Rarb2, were colocalized in stromal mesenchyme, a third renal cell type, where their deletion led to altered stromal cell patterning, impaired ureteric bud growth and downregulation of Ret in the ureteric bud. Here we demonstrate that forced expression of Ret in mice deficient for both Rara and Rarb2 (Rara(-/-)Rarb2(-/-)) genetically rescues renal development, restoring ureteric bud growth and stromal cell patterning. Our studies indicate the presence of a new reciprocal signaling loop between the ureteric bud epithelium and the stromal mesenchyme, dependent on Ret and vitamin A. In the first part of the loop, vitamin-A-dependent signals secreted by stromal cells control Ret expression in the ureteric bud. In the second part of the loop, ureteric bud signals dependent on Ret control stromal cell patterning. 相似文献