lab gene expression is driven heat shock promoter.
Heat induced expression does not affect tarsal leg structures but causes some thickening of the arista.
Heat shocked labhs.PH larvae lack sclerotic plates but differentiate in every thoracic and abdominal segment a stereotyped arch-shaped cephalic structure which appears in the ventral region and results from the fusion of material at the left and right sides.
Heat shock treatments between 7 and 9 hours of embryonic development generate extra copper cells posterior to the normal copper cell domain in the larval midgut. Large flat cells and interstitial cells are transformed into cuprophilic cells. This effect is dependent on endogenous lab function. Heat shock after 11 hours of development generates cuprophilic cells with 'banana shapes' abnormally near the anterior margin of the copper cell domain. A single heat pulse between 9 and 11 hours of development frequently results in severe or virtually complete repression of copper cell development, indicating that lab autoregulation in the midgut can be negative.
Double antibody staining with F2 and P12α-85E revealed the T1-T3 es organs to be abnormal, lch5 abnormal in some A segments and dch3 partially transformed to lch3 in T2 and T3.
labhs.PH is a suppressor of embryonic epidermis phenotype of Abd-BM8, AntpNs-rvC3, ScrC1, UbxMX2, abd-AM1
labhs.PH, ssaSc has tarsal segment phenotype
labhs.PH, ssaSc has antennal segment phenotype
labhs.PH, ssa40aw has third segment of antenna phenotype
Induction of expression in ssaSc flies causes shortening of tarsi in all antennal and leg structures. Third segment of the antenna exhibits a multiple bristle phenotype. Induction of expression in ssa40aw flies causes overgrowth of the third antennal segment without the formation of multiple bristles.
ScrC1 AntpNs-rvC3 UbxMX2 abd-AM1 Abd-BM8 larvae (deficient for activity of thoracic and abdominal homeotic genes) exhibit sclerotic plates anterior to each denticle belt. Expression of labhs.PH suppresses the differentiation of the sclerotic plates. The appearance of the sclerotic plates seen in heat shocked labhs.PH larvae can suppressed by any homeotic gene.
Expression of labhs.PH between 5 and 6 hours of development (using heat shock) rescues the embryonic brain defects of lab9 animals; the tritocerebral commissure is restored (although it is thinner than in wild-type animals) and the longitudinal connectives are also present. Some variability in rescue is seen; approximately 85% of embryos show essentially complete restoration of the tritocerebral commissure and longitudinal connectives, 10% of embryos lack a normal tritocerebral commissure but have unfasciculated axons where this structure should be, and 5% of embryos show no rescue. Expression of labhs.PH at 4-5 hours and 6-7 hours of development (using heat shock) rescues the lab9 phenotype in approximately 10% of embryos. No rescue is seen in embryos heat shocked at 7-8, 8-9, 9-10 or 10-11 hours of development.
