Spermatogenesis in XO,Sxr mice: Role of the Y chromosome

Abstract

The goal of this investigation was to evaluate the role of the Y chromosome in spermatogenesis by a quantitative and qualitative analysis of spermatogenesis as it occurs in the absence of a significant portion of the Y chromosome, i.e., in XO,Sxr male mice. Although these mice have the testis-determining portion of the Y chromosome on their single X chromosome, they lack most of the Y chromosome. Since it was found that all sperm-specific structures were assembled in a normal spatial and temporal pattern in spermatids of XO,Sxr mice, the genes controlling these structures cannot be located on the Y chromosome outside of the Sxr region, and are more likely to be on autosomes or on the X chromosome. In spite of the assembly of the correct sperm-specific structures, spermatogenesis was not quantitatively normal in XO,Sxr mice and significantly reduced numbers of spermatids were found in the seminiferous tubules of these mice. Furthermore, two size classes of spermatids were found in the testes of XO,Sxr mice, normal and twice-normal size. These findings are suggestive of abnormalities of meiosis in XO,Sxr spermatocytes, which lack one of the two sex chromosomes, and may not implicate function of specific genes on the Y chromosome. Morphological abnormalities of spermatids, which were not unique to XO,Sxr mice, were observed and these may be due to either a defective testicular environment because of reduced numbers of germ cells or to the lack of critical Y chromosome-encoded products. Since pachytene spermatocytes of XO,Sxr mice exhibited a sex vesicle, it can be concluded that the assembly of this structure does not depend on the presence of either a complete Y chromosome or the pairing partner for the X chromosome.

The Aurora kinase inhibitor ZM447439 accelerates first meiosis in mouse oocytes by overriding the spindle assembly checkpoint

“…Assuming the SAC to be present in oocytes, one would have anticipated a cell arrest due to a failure in generating tension across the one remaining sister kinetochore pair, and indeed this is observed in the sex-reversed XO male mouse (Kot & Handel 1990, Sutcliffe et al 1991. It would be possible for the SAC to be satisfied if the X chromosome divided as it does in meiosis II; indeed, such equational divisions can occur in meiosis I when mice lack the synaptonemal complex component SYCP3 (Kouznetsova et al 2007).…”

Evidence that sex chromosome asynapsis, rather than excess Y gene dosage, is responsible for the meiotic impairment of XYY mice

“…In particular, XSxr a O males (in which the X chromosome carries a small portion of the short arm of the Y chromosome, including the sex-determining gene Sry [Gubbay et al, 1990]) have provided a valuable model for studying the effect of sex chromosome asynapsis on spermatogenesis. These animals are sterile owing to an almost total spermatogenic block at the first meiotic metaphase stage (MI) (Kot and Handel, 1990;Sutcliffe et al, 1991); any sperm that are produced are grossly abnormal and frequently diploid (Levy and Burgoyne, 1986). However, when an Y* X chromosome, comprising a pseudoautosomal region (PAR) attached to a non-Y centromere, lacking any Y-specific DNA Burgoyne et al, 1998) was provided as a synaptic partner for the XSxr a chromosome, the meiotic block was overcome (Burgoyne et al, 1992).…”

Mouse Y-Linked Zfy1 and Zfy2 Are Expressed during the Male-Specific Interphase between Meiosis I and Meiosis II and Promote the 2nd Meiotic Division

“…Paradoxically, in both Eif2s3y rescue models the majority of spermatocytes complete meiosis I, whereas in the X Sxr a O ‘control’ there is a very efficient apoptotic elimination of spermatocytes at the first meiotic metaphase (MI) [9]–[11]; this apoptosis is assumed to be triggered by an MI spindle assembly checkpoint (SAC) response to the univalent X at MI [12]. This suggested that a Yp gene that was deleted or inactivated in Sxr b was necessary for an efficient apoptotic response to the univalent X, although a markedly reduced apoptotic response remained.…”