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Tumorous-head (tuh-1; tuh-3) modulates Abd-B bithorax-complex functions in Drosophila melanogaster.

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Abstract Abdominal-B (Abd-B) mutants of the bithorax-complex (BX-C) were studied in trans with tuh-3 to evaluate their interactions with this homeotic mutant and the maternal effect locus (tuh-1) controlling tuh-3 expression. Head defects occur in tuh-3 offspring from tuh-1h homozygous mothers, while genital defects occur in homozygous tuh-3 offspring from mothers carrying the tuh-1g allele. The influence exerted by the tuh-1 maternal effects on tuh-3 Abd-B transcript distribution was evaluated by whole mount in situ hybridization. Results demonstrated that: (1) of the 21 Abd-B mutants tested, head defects were produced by SGA62, I127B, I127O and tuh-3, with I127B and tuh-3 as the only mutants to require the head defect maternal effect for expression; (2) one specific cluster of regulatory (r) mutants, Uab1, 65 and I127B, enhanced penetrance and expressivity of tuh-3 head defects; (3) the most profound suppression of head defect penetrance occurred when Abd-B mutants eliminated the morphogenetic (m) and r functions; (4) genital defects increased in frequency in tuh-3/Abd-B mutant trans-heterozygotes with loss of r function; (5) Abd-B transcription (class A, class B, class C) appears normal in tuh-3 embryos when their mothers pass on the tuh-1h head defect maternal effect, whereas the regulatory transcripts (class B and class C) are reduced when tuh-3 mothers pass on the tuh-1g genital disc maternal effect; (5) tuh eye-antennal imaginal discs express ABD-B protein; and (6) tuh-3 misregulates both m and r function of Abd-B.
Title: Tumorous-head (tuh-1; tuh-3) modulates Abd-B bithorax-complex functions in Drosophila melanogaster.
Description:
Abstract Abdominal-B (Abd-B) mutants of the bithorax-complex (BX-C) were studied in trans with tuh-3 to evaluate their interactions with this homeotic mutant and the maternal effect locus (tuh-1) controlling tuh-3 expression.
Head defects occur in tuh-3 offspring from tuh-1h homozygous mothers, while genital defects occur in homozygous tuh-3 offspring from mothers carrying the tuh-1g allele.
The influence exerted by the tuh-1 maternal effects on tuh-3 Abd-B transcript distribution was evaluated by whole mount in situ hybridization.
Results demonstrated that: (1) of the 21 Abd-B mutants tested, head defects were produced by SGA62, I127B, I127O and tuh-3, with I127B and tuh-3 as the only mutants to require the head defect maternal effect for expression; (2) one specific cluster of regulatory (r) mutants, Uab1, 65 and I127B, enhanced penetrance and expressivity of tuh-3 head defects; (3) the most profound suppression of head defect penetrance occurred when Abd-B mutants eliminated the morphogenetic (m) and r functions; (4) genital defects increased in frequency in tuh-3/Abd-B mutant trans-heterozygotes with loss of r function; (5) Abd-B transcription (class A, class B, class C) appears normal in tuh-3 embryos when their mothers pass on the tuh-1h head defect maternal effect, whereas the regulatory transcripts (class B and class C) are reduced when tuh-3 mothers pass on the tuh-1g genital disc maternal effect; (5) tuh eye-antennal imaginal discs express ABD-B protein; and (6) tuh-3 misregulates both m and r function of Abd-B.

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