Fusion of B-H1 to heat shock promoter.
Overexpression during late-second instar to the end of the third instar frequently induces B-like eye malformation or reduced eye morphology due to suppression of ommatidial differentiation. The number of eliminated ommatidia decreases the later the heat induced overexpression of B-H1, this data suggests overexpression induces cessation of the anterior progression of the morphogenetic furrow in the eye disc. At the anterior edge of malformed eyes isolated sensilla can be seen suggesting homeotic transformation of trichoid to campaniform-like sensilla. Overexpression during early-third-instar larvae causes the ommatidial area to be divided into two or three areas by scars. Scars are formed by elimination of about 10 columns of ommatidia. Scar formation is brought about by temporal interruption of anterior movement of the morphogenetic furrow. Heavy pigmentation occurs in the region corresponding to the stopped morphogenetic furrow. 1-6 columns posterior to the stopped morphogenetic furrow 5-50% ommatidia exhibit morphological abnormality, including reduction in photoreceptor number, conversion of photoreceptor types and aberrant ommatidial orientation.
Overexpression of B-H1 causes almost complete conversion of trichoid to campaniform-like sensilla, this does not require endogenous B-H2.
Transient overexpression of B-H1 in late third instar larvae caused eye malformation: decrease in ommatidia.