Spermatocyte apoptosis, which involves intrinsec aand extrinsec pathways, explains the sterility of Graomys griseoflavus x Graomys centralis mice male hybrids

RODRIGUEZ V; DÍAZ DE BARBOZA G; PONCE R; MERICO V; GARAGNA S; TOLOSA DE TALAMONI N

REPRODUCTION FERTILITY AND DEVELOPMENT

Csiro Publishing

Lugar: Collingwood, Australia; Año: 2010 vol. 22 p. 478 - 488

1031-3613

Spermatogenic impairment and apoptotic pathways involved in establishing sterility of male hybrids obtained from crossing Graomys griseoflavus females with Graomys centralis males were studied. Testes from G. centralis, G. griseoflavus and hybrids were compared at different ages. TUNEL, Fas, Bax and cytochrome c labeling were used for apoptosis evaluation and calbindin D28k staining as an anti-apoptotic molecule. In 1-month-old animals, spermatocytes were positive for all apoptotic markers, but moderate TUNEL (+) spermatocyte frequency was only found in G. centralis. At subsequent ages, the apoptotic markers were down-regulated in testes from parental cytotypes, but not in hybrid testes. TUNEL (+) spermatocytes were 78% and 44%/tubule cross section in 2- and 3-month-old hybrid animals, respectively. Pachytene spermatocyte death in adult hybrids occurs via apoptosis, as revealed by high caspase-3 expression. Calbindin was highly expressed in spermatocytes of adult hybrids, in which massive cell death occurs via apoptosis. Calbindin co-localisation with TUNEL or Fas, Bax and cytochrome c was very limited, suggesting an inverse regulation of calbindin and apoptotic markers. The hybrid sterility is due to breakdown of spermatogenesis at the pachytene spermatocyte stage. Both extrinsic and intrinsic pathways are involved in apoptosis of spermatocytes, which are the most sensitive cell type to apoptotic stimuli.