Spermatogenesis is a hormonally regulated process involving three sequential events: (1) the mitotic amplification of the spermatogonial cell progeny, (2) the completion of meiosis by the spermatocyte progeny, and (3) spermiogenesis, the gradual morphogenesis of the spermatid progeny. Mitosis, meiosis and spermiogenesis coexist in the seminiferous epithelium in association with a post-mitotic stable population of somatic Sertoli cells. Cell components of each spermatogonial, spermatocyte, and spermatid cell progeny remain connected by intercellular cytoplasmic bridges. Intercellular bridges are disrupted upon completion of spermiogenesis leading to the release in the seminiferous tubular lumen of single mature spermatids transported to the epididymal duct for acquisition of fertilizing activity. Several key cell cycle regulators have been shown to operate during the mitotic amplification of the spermatogonial progeny. During meiotic prophase, autosomal bivalents are engaged in prominent ribosomal RNA and non-ribosomal RNA transcriptional activity, in contrast with the transcriptional silencing of the condensed XY chromosomes. An autosomal bivalent is a synapsed (conjoined) chromosomal pair, excluding the sex chromosomes X and Y, observed during meiotic prophase I. Each member of a chromosomal bivalent (autosomes and X-Y) consists of two sister chromatids that will disjoin (separate) upon completion of meiosis to produce a haploid genome (spermatid). During spermiogenesis, gradual genetic inactivation of the spermatid genome correlates with spermatid head shaping. The acrosome-acroplaxome-manchette complex is emerging as a significant player in spermatid head shaping as well as in the assembly of the sperm head–tail coupling apparatus and the development of the outer dense fiber-axoneme-containing sperm tail. The acroplaxome is a cytoskeletal plate bordered by a desmosome-like marginal ring fastening the descending recess of the acrosomal sac to the nuclear envelope of the spermatid. The manchette is a transient microtubular-containing structure developed beneath the acroplaxome and encircling the elongating spermatid nucleus. This chapter is restricted to recent developments in the bioregulation of the spermatogonial stem cell progeny, the process of transcriptional inactivation of the XY bivalent, and the steps leading to spermatid head shaping. These are three relevant aspects that, when disrupted, can lead to male infertility.
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Editors and Affiliations
- ATR:
-
DNA repair protein, member of the PI3-kinase-like family
- Brca1:
-
breast cancer 1 gene
- c-kit:
-
cellular homolog of the feline sarcoma viral oncogene v-kit
- cyclin D1 and D2:
-
cell cycle-regulatory genes
- DSB:
-
double-strand breaks
- FSH:
-
follicle stimulating hormone
- GDNF:
-
glial cell line-derived neurotrophic factor
- GOPC:
-
Golgi-associated PDZ and coiled-coil motif containing
- H2AFY:
-
H2A histone family, member Y (also known as histone macroH2A1)
- H2AX:
-
variant of the histone H2a
- Hrb:
-
Asn-Pro-Phe (NPF) motif-containing protein (also called Rab or hRip)
- hRip:
-
human immunodeficiency virus Rev-interacting protein.
- KIFC:
-
kinesin family member C
- MANO:
-
meiotic autosomal nucleolar organization
- MCSI:
-
meiotic sex chromosome inactivation
- Mre11:
-
meiotic recombination 11 protein
- Nbs1:
-
Nijmegen breakage syndrome 1
- ODF2:
-
Outer dense fiber 2
- Plzf:
-
promyelocytic leukemia zinc-finger, a transcriptional repressor encoded by the Zfp145 gene
- POK:
-
Poxviruses and zinc-finger (POZ) and Krüppel family of transcription repressors
- POZ:
-
Poxviruses and zinc-finger
- Rab:
-
member of the Ras superfamily of monomeric G proteins
- Rad3:
-
a DNA helicase repair protein
- Rad50:
-
Mre11-interacting protein with binding affinity to double stranded DNA.
- RET:
-
protooncogene tyrosine kinase receptor that binds members of the GDNF family
- Ssty 1 and Ssty 2:
-
Y-linked spermiogenesis specific transcript
- Zfp145:
-
zinc finger protein 145 gene
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Tres, L.L., Kierszenbaum, A.L. (2009). The Molecular Landscape of Spermatogonial Stem Cell Renewal, Meiotic Sex Chromosome Inactivation, and Spermatic Head Shaping. In: Chedrese, P. (eds) Reproductive Endocrinology. Springer, Boston, MA. https://doi.org/10.1007/978-0-387-88186-7_27
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