P{lacW} insertion in the 5' untranslated region.
Adult males have very small testes, they are almost completely devoid of germ cells. Rare spermatocytes and some scarce nonmotile sperm are seen. Females exhibit oogenic defects: block of oogenesis around stage 6 or 7 leading to the accumulation of egg chambers showing several striking defects, or late defects including short and/or flaccid eggs showing fused, short or no dorsal appendage.
SxlM12, noi2/noiD has male sterile phenotype, non-enhanceable by snf+t5.5
SxlM12, noi2/noiD has male sterile phenotype, non-suppressible by snf+t5.5
noi2/noiD is a non-suppressor of male sterile phenotype of SxlM12
noi2/noiD is a non-suppressor of abnormal developmental rate | male phenotype of SxlM12
The removal of noi function (by adding noi2/noiD) leads to an almost complete suppression of the foreleg feminisation phenotype seen in SxlMf1/Y flies with two copies of P{snf+,dhd+}. The addition of two copies of P{snf+,dhd+} to SxlMf1/Y males that also carry noi2/noiD, leads to feminisation of the foreleg and a reduction in viability. The addition of noi2/noiD does not suppress the snf+t5.5 dose effects on SxlM12/Y male viability. The addition of P{snf+,dhd+} has no effect on the male sterility and developmental delay phenotypes seen in noi2/noiD, SxlM12/Y males.
All aspects of the phenotype can be rescued by noi+t3.6.
Reversion of the P{lacW} insertion demonstrates it is responsible for the mutant phenotype.