Q240term | sens-PA
The nucleotide change was reported in the context of surrounding sequence but on the negative strand.
sensE2/+ results in an approximately 35% reduction in the loss of wing margin caused by mir-9aJ22/mir-9aE39. sensE2/+ does not rescue the increased cell death seen in the wing discs of mir-9aJ22/mir-9aE39 animals.
sc10-1; sensE2/+ flies show a severe loss of stout bristles at the wing margin in comparison to sc10-1 single mutants, which show a small loss of these bristles. At the pupal level the sc10-1; sensE2/+ double mutants are almost completely lacking the neurons that should have developed from the mechanosensory precursors; this is an enhancement of the reduced number of neurons seen in sc10-1 single mutant pupae. The double mutants also show a greater loss of socket cells than the single mutants.
Thoracic clones that express daScer\UAS.cGa, under the control of Scer\GAL4tub, in a sensE2 background results in clones that lack microchaetae. Sensory organ precursors in these clones generate extra neurons but no shaft or socket cells, which is similar to sensE2 single mutant clones.
In rho7M43; ru1; sensE2 triple mutant clones, no photoreceptors differentiate except for a few photoreceptors near the clonal boundary, presumably rescued non-autonomously by neighboring wild-type cell. No rescue of photoreceptor development is seen when these triple mutant clones are made in a rox63 homozygous background. Adult eyes containing sensE2 homozygous somatic clones induced in an EgfrE1/+ background are smaller than wild-type. Within the clone there are reduced numbers of ommatidia, as well as gaps of tissue between ommatidia, a phenotype similar to that seen in EgfrE1 homozygotes.
When Df(3L)H99 (A deficiency that uncovers grim, rpr and W) is combined with sensE2, 93% of salivary glands are normal in size (compared with 0% for sensE2 mutants). The addition of W05014 or Df(3L)XR38 (which removed rpr) partially suppresses this phenotype as well, though the suppression by W05014 is quantitatively and qualitatively weaker than Df(3L)XR38.
Expression of sens1CCg does not rescue the lethality of sensE2 homozygous embryos. However, a significant rescue of PNS development is observed. The rescue is however, not complete, as some of the neurons are lost. In addition, the neurons exhibit differentiation, axon guidance, and fasciculation defects.