Is the sperm centrosome to blame for the complex polyploid chromosome patterns observed in cleavage stage embryos from an OAT patient?

• Published in: Zygote (Cambridge) Vol. 15; no. 1; p. 81
• Main Authors: Chatzimeletiou, K, Rutherford, A J, Griffin, D K, Handyside, A H
• Format: Journal Article
• Language: English
• Published: England 01-02-2007
• Subjects: Adult; Asthenozoospermia - genetics; Centrosome - ultrastructure; Cleavage Stage, Ovum - ultrastructure; Embryonic Development - genetics; Female; Humans; In Situ Hybridization, Fluorescence; In Vitro Techniques; Male; Models, Genetic; Oligospermia - genetics; Polyploidy; Sperm Injections, Intracytoplasmic; Spermatozoa - ultrastructure
• ISSN: 0967-1994
• DOI: 10.1017/S0967199406004059

Oligoasthenoteratozoospermia (OAT) is defined by a combined low count < 20 x 10(6) sperm/ml, poor motility < 50 % forward progression or < 25 % rapid linear progression and abnormal morphology (5-8 % normal using Kruger strict criteria) and has been associated with increased levels of sperm aneuploidy. Here we report on the cytogenetic findings from three 'spare' embryos from a couple that were referred for ICSI because of OAT. The embryos were processed for sequential FISH in three hybridization rounds using probes for chromosomes 3, 7, 9, 13, 17, 18, 21, X and Y. Molecular cytogenetic analysis of nine chromosomes revealed that all three embryos were female polyploid. One of them was uniformly tetraploid for all chromosomes tested, while the remaining two embryos showed evidence of abnormal postzygotic segregation of chromosomes, causing the derivative blastomeres to have uneven chromosomal constitution. In one of them in particular, the non-disjoining chromosomes showed preferential segregation to the same pole, rather than randomly moving towards either pole, suggesting an abnormal spindle and causing the derivative blastomeres to have significantly uneven chromosomal constitutions. The possible scenarios leading to polyploidy and chromosomal imbalance through cytokinetic failure and subsequent abnormal centrosomal distribution are outlined.