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Spermatid Development (spermatid + development)
Selected AbstractsRnf19a, a ubiquitin protein ligase, and Psmc3, a component of the 26S proteasome, Tether to the acrosome membranes and the head,tail coupling apparatus during rat spermatid developmentDEVELOPMENTAL DYNAMICS, Issue 7 2009Eugene Rivkin Abstract We report the cDNA cloning of rat testis Rnf19a, a ubiquitin protein ligase, and show 98% and 93% protein sequence identity of testicular mouse and human Rnf19a, respectively. Rnf19a interacts with Psmc3, a protein component of the 19S regulatory cap of the 26S proteasome. During spermatid development, Rnf19a and Psmc3 are initially found in Golgi-derived proacrosomal vesicles. Later on, Rnf19a, Psmc3, and ubiquitin are seen along the cytosolic side of the acrosomal membranes and the acroplaxome, a cytoskeletal plate linking the acrosome to the spermatid nuclear envelope. Rnf19a and Psmc3 accumulate at the acroplaxome marginal ring,manchette perinuclear ring region during spermatid head shaping and in the developing sperm head,tail coupling apparatus and tail. Rnf19a and Psmc3 may interact directly or indirectly with each other, presumably pointing to the participation of the ubiquitin,proteasome system in acrosome biogenesis, spermatid head shaping, and development of the head-tail coupling apparatus and tail. Developmental Dynamics 238:1851,1861, 2009. © 2009 Wiley-Liss, Inc. [source] Role of cell adhesion molecule nectin-3 in spermatid developmentGENES TO CELLS, Issue 9 2006Maiko Inagaki First page of article [source] cAMP response element modulator (CREM): an essential factor for spermatogenesis in primates?INTERNATIONAL JOURNAL OF ANDROLOGY, Issue 3 2001R. Behr CREM is a cAMP-related transcription factor and alternate promotor usage and splicing generate repressor and activator transcripts of CREM within the testis. CREM activators are highly expressed in post-meiotic haploid germ cells and are essential for spermatid maturation in the mouse model as revealed by gene-targeting studies. Analysis of testicular CREM expression in rodent and monkey species, and in men yielded a highly comparable pattern thus suggesting that CREM is of general importance for spermatid development in the mammalian testis. Also, many CREM target genes have been identified in haploid germ cells. Studies in men with spermatogenic disturbance and spermatid maturation arrest demonstrated abnormal CREM expression and altered splicing events. Collectively, the data strongly argue for an essential role of CREM during spermatid maturation in primates. [source] Alterations in the testis of hormone sensitive lipase-deficient mice is associated with decreased sperm counts, sperm motility, and fertilityMOLECULAR REPRODUCTION & DEVELOPMENT, Issue 4 2008Louis Hermo Abstract Hormone-sensitive lipase (HSL, Lipe, E.C.3.1.1.3) functions as a triglyceride and cholesteryl esterase, supplying fatty acids, and cholesterol to cells. Gene-targeted HSL-deficient (HSL,/,) mice reveal abnormal spermatids and are infertile at 24 weeks after birth. The purpose of this study was to follow the evolution of spermatid abnormalities as HSL,/, mice age, characterize sperm motility in older HSL,/, mice, and determine if mice expressing a human testicular HSL transgene (HSL,/,ttg) produce normal motile sperm. In situ hybridization indicated that HSL is expressed exclusively in steps 5,16 spermatids, but not in Sertoli cells. In HSL,/, mice, abnormalities were evident in step 16 spermatids at 5 weeks after birth, with defects progressively increasing in spermatids with age. The defects included multinucleation of spermatids, abnormal shapes and a reduction of elongating spermatids. In older HSL,/, mice, sperm counts appeared reduced by 42%, but this value was lower because samples were compromised by the presence of small degenerating germ cells in addition to sperm, both of which appeared of similar size and density. Sperm motility was dramatically reduced with only 11% classified as motile in HSL,/, mice compared to 76,78% of sperm in wild-type and HSL,/,ttg mice. Sperm morphology, counts, and motility were normal in HSL,/,ttg mice, as was their fertility. Collectively, the data indicate that HSL deficiency results in abnormal spermatid development with defects arising at 5 weeks of age and progressively increasing at later ages. HSL,/, mice also show a dramatic reduction in sperm counts and motility and are infertile. Mol. Reprod. Dev. 75: 565,577, 2008. © 2007 Wiley-Liss, Inc. [source] | ||||||||||