Dear Editor

The high incidence of spermatocyte apoptosis described in infertile men is largely attributable to chromosomal asynapsis and underscores the need for better animal models to understand how damaged meiotic germ cells are selectively eliminated.1 We have previously inactivated the Scp3 gene (also known as Cor1) in mice, which encodes a major structural component of the axial/lateral element of the synaptonemal complex (SC).2 The spermatocytes in these null animals exhibit extensive chromosomal asynapsis at an early meiotic stage and undergo apoptosis. Several mechanisms may mediate this selective apoptotic response. For example, it is known that p53 is required for checkpoint-induced apoptosis in male germ cells in response to irradiation1 and in response to loss of the ataxia-telangiectasia protein (ATM).3,4

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