About: Spermatid is a research topic. Over the lifetime, 2124 publications have been published within this topic receiving 72716 citations. The topic is also known as: spermatids.
TL;DR: It is concluded that cell-autonomous action of the AR in SC is an absolute requirement for androgen maintenance of complete spermatogenesis, and that sPermatocyte/spermatid development/survival critically depends on androgens.
Abstract: Androgens control spermatogenesis, but germ cells themselves do not express a functional androgen receptor (AR). Androgen regulation is thought to be mediated by Sertoli and peritubular myoid cells, but their relative roles and the mechanisms involved remain largely unknown. Using Cre/loxP technology, we have generated mice with a ubiquitous knockout of the AR as well as mice with a selective AR knockout in Sertoli cells (SC) only. Mice with a floxed exon 2 of the AR gene were crossed with mice expressing Cre recombinase ubiquitously or selectively in SC (under control of the anti-Mullerian hormone gene promoter). AR knockout males displayed a complete androgen insensitivity phenotype. Testes were located abdominally, and germ cell development was severely disrupted. In contrast, SC AR knockout males showed normal testis descent and development of the male urogenital tract. Expression of the homeobox gene Pem, which is androgen-regulated in SC, was severely decreased. Testis weight was reduced to 28% of that in WT littermates. Stereological analysis indicated that the number of SC was unchanged, whereas numbers of spermatocytes, round spermatids, and elongated spermatids were reduced to 64%, 3%, and 0% respectively of WT. These changes were associated with increased germ cell apoptosis and grossly reduced expression of genes specific for late spermatocyte or spermatid development. It is concluded that cell-autonomous action of the AR in SC is an absolute requirement for androgen maintenance of complete spermatogenesis, and that spermatocyte/spermatid development/survival critically depends on androgens.
TL;DR: Comparison of protamine gene and amino-acid sequences suggests that the family evolved from specialized histones through protamine-like proteins to the true protamines.
Abstract: The protamines are a diverse family of small arginine-rich proteins that are synthesized in the late-stage spermatids of many animals and plants and bind to DNA, condensing the spermatid genome into a genetically inactive state. Vertebrates have from one to 15 protamine genes per haploid genome, which are clustered together on the same chromosome. Comparison of protamine gene and amino-acid sequences suggests that the family evolved from specialized histones through protamine-like proteins to the true protamines. Structural elements present in all true protamines are a series of arginine-rich DNA-anchoring domains (often containing a mixture of arginine and lysine residues in non-mammalian protamines) and multiple phosphorylation sites. The two protamines found in mammals, P1 and P2, are the most widely studied. P1 packages sperm DNA in all mammals, whereas protamine P2 is present only in the sperm of primates, many rodents and a subset of other placental mammals. P2, but not P1, is synthesized as a precursor that undergoes proteolytic processing after binding to DNA and also binds a zinc atom, the function of which is not known. P1 and P2 are phosphorylated soon after their synthesis, but after binding to DNA most of the phosphate groups are removed and cysteine residues are oxidized, forming disulfide bridges that link the protamines together. Both P1 and P2 have been shown to be required for normal sperm function in primates and many rodents.
TL;DR: Results from the studies indicate that changes in the metabolism of proteins lipids and carbohydrates take place in the testes under the control of hormones, but it may be that the observed biochemical changes are a reflection of the changes in cellular composition of testicular tissue rather than the result of metabolic changes within a specific cell type in response to the effect of a hormone.
Abstract: Studies of the hormonal control of the spermatogenic process are reviewed. Most of the investigations used the techniques of ablation and replacement therapy and were performed on the rat. Results from the studies indicate that changes in the metabolism of proteins lipids and carbohydrates take place in the testes under the control of hormones. However it may be that the observed biochemical changes which occur are a reflection of the changes in cellular composition of testicular tissue rather than the result of metabolic changes within a specific cell type in response to the effect of a hormone. A hypothesis concerned with the qualitative aspects of hormonal control of spermatogenesis in the rat has been formed. It is proposed that the multiplication and growth of gonocytes prenatally and in the first few days after birth and formation of type A spermatogonia are under the control of testosterone. The formation of type A and B spermatogonia and primary spermatocytes and progression of the meiotic prophase may be influenced by growth hormone. Reduction division is under control of testosterone. The early steps of spermatid formation may be under no hormonal control or may require testosterone while the late stages of spermatid maturation require the presence of FSH.
TL;DR: The Drosophila melanogaster fuzzy onions fzo gene encodes the first known protein mediator of mitochondrial fusion, a large, novel, predicted transmembrane GTPase that becomes detectable on spermatid mitochondria late in meiosis II, just prior to fusion, and disappears soon after fusion is complete.
TL;DR: It is shown that apoptotic proteins play an essential role during spermatid individualization in Drosophila melanogaster, and that a giant ubiquitin-conjugating enzyme, dBruce, is required to protect the sperm nucleus against hypercondensation and degeneration.