Two states of active spermatogenesis switch between reproductive and non-reproductive seasons in the testes of the medaka, Oryzias latipes.

Seasonal change in spermatogenesis was examined in the restricted spermatogonium-type testes of a teleost, Oryzias latipes. Histological observation revealed that the number of each stage of germ cells during most of the non-reproductive season, from October to January (O-J period) was nearly half of that during the reproductive season, from May to July (M-J period), except for type B spermatogonia (B-gonia), which was actually equal. As a result, the ratio of primary spermatocytes (P-cytes) to B-gonia was remarkably small in the O-J period. Despite the differences between both time periods, the proliferative activity of type A spermatogonia (A-gonia), B-gonia, or P-cytes was at a similar level in both periods. Moreover, in cultured testes treated with bromodeoxyuridine as a cell-lineage tracer, P-cytes differentiated to spermatids in 11-15 days in both M-J and O-J periods. These indicate that spermatogenesis is active in each period at a different state. In the spermatogenic testis, A-gonial proliferation was maintained by human follicle stimulating hormone/luteinizing hormone in culture. Whereas cell death of B-gonia and/or P-cytes gradually increased in the M-J period in spite of those cells being constant in population sizes. In transition to the O-J period, A-gonia and P-cytes first decreased, which was accompanied by a decrease in proliferative activity of A-gonia and relative increase of dead cells from B-gonia and/or P-cytes against live P-cytes. These suggest that A-gonial proliferation and cell death of B-gonia and/or P-cytes that is induced coordinately with B-gonial differentiation are critical for the spermatogenic control.

A wide-range phylogenetic analysis of Zic proteins: implications for correlations between protein structure conservation and body plan complexity.

We compared Zic homologues from a wide range of animals. Striking conservation was found in the zinc finger domains, in which an exon-intron boundary has been kept in all bilateralians but not cnidarians, suggesting that all of the bilateralian Zic genes are derived from a single gene in a bilateralian ancestor. There were additional conserved amino acid sequences, ZOC and ZF-NC. Combined analysis of the zinc finger, ZOC, and ZF-NC revealed the presence of two classes of Zic, based on the degree of protein structure conservation. The "conserved" class includes Zic proteins from the Arthropoda, Mollusca, Annelida, Echinodermata, and Chordata (vertebrates and cephalochordates), whereas the "diverged" class contains those from the Platyhelminthes, Cnidaria, Nematoda, and Chordata (urochordates). The result indicates that the ancestral bilateralian Zic protein had already acquired an entire set of conserved domains, but that this was lost and diverged in the platyhelminthes, nematodes, and urochordates.

The effects of dietary vitamin B12 deficiency on sperm maturation in developing and growing male rats.

To evaluate the role of vitamin B12 on spermatogenesis, the effects of dietary vitamin B12 deficiency on sperm maturation in developing rat fetuses and young growing rats were examined. The vitamin B12-deficient diet was given to all the animals for three different periods: whole period (gestation to mature), gestation period (gestation to weaning), or immature period (3-12 weeks postnatal). Sperm examination revealed that the sperm count was markedly lower in male progeny (F1) that were vitamin B12-deficient during the whole period. In addition, a significantly higher number of abnormal sperm, such as tailless and amorphous sperm, was observed. In male rats that were vitamin B12-deficient during the immature period, the incidence of abnormal sperms was 14.4% and 4.8% for tailless and short tail, respectively. The motion rates, such as path velocity and straight line velocity, were decreased to 20-40% of the control value in rats that were vitamin B12-deficient both during the whole and gestation periods. However, no effects of vitamin B12 deficiency on sperm motility were observed during the immature and mature periods. From these findings, we suggest that dietary vitamin B12 deficiency during pregnancy may induce irreversible damage in the germ cells of embryos and affect the maturation of spermatozoa.