A deletion from 92 nucleotides upstream of the start codon to 117 nucleotides upstream of the stop codon of noi.
Homozygous embryonic development is completely normal but the embryos fail to hatch. noi+t3.6 cannot rescue the homozygous lethality.
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.
"noi1" was stated as tentative. "noi2" was stated as tentative. It is not known if the homozygous lethality is due to deletion of another essential gene or if the chromosome bears another lethal mutation elsewhere.