4bp deletion in the Prosα6T sequence, producing a frameshift mutation at codon 115, which should result in a translation stop occurring 41 codons later.
nucleus & elongation stage spermatid
The testes of homozygous males are of normal size and shape, but there are no mature sperm in the seminal vesicle. All stages of spermatogenesis up through spermatid elongation appear normal in the mutant males, however, there are defects in sperm individualisation, resulting in few, if any, mature motile sperm.
Defects in nuclear morphological changes are seen during spermatid bundle elongation in mutant males; some nuclei do not fully condense, some are scattered and some lose the rigid needle-like shape and appear curled, and in many cases contorted into circles. The defects become more severe in older males, with an increase in scattered nuclei.
The initial assembly of the actin cones of the individualization complex and their triangular shape is normal in mutant males. However, the coordinated movement of these cones is disrupted in the mutant males, with the disruption becoming more extreme as the cones move further down the spermatid bundles.
Prosα6T1 has male sterile | recessive phenotype, suppressible by Prosα6Prosα3T.PZ
Expression of Pros35Prosα3T.PZ completely rescues the sterility of Prosα6T1 mutant males.
Prosα6T1 is rescued by Prosα6TEGFP