The tumorous-head-1 locus affects bristle number of the Drosophila melanogaster cuticle.

The tuh-1 maternal effect locus contains two naturally occurring isoalleles, tuh-1h and tuh-1g. Until recently there has been no possibility to distinguish between the tuh-lh and the tuh-1g maternal effects other than evaluating their effect on the Bithorax-Complex (BXC) Abdominal B (Abd-B) mutant tuh-3. However, in this report we identify a bristle phenotype associated with the tuh-1 locus that has very interesting evolutionary implications. Females homozygous for tuh-1h always produce adult offspring with more bristles than females homozygous or heterozygous for tuh-1g. The effect is global. Increased bristle number occurs in the head, the thorax, and the anterior and posterior abdomen. Females totally deficient for the tuh-1 gene produce offspring with high bristle number. Thus, the bristle phenotype results from the absence of the maternally contributed tuh-1g factor. Genetic evidence shows that the bristle phenotype is caused by the tuh-1 locus and that tuh-1h is completely recessive to tuh-1g. The tuh-1 locus is located at the euchromatin-beta-heterochromatin junction near the centromere of the X chromosome and deficiency analysis places the locus between the lethal genes extra organs (eo) and lethal B20 (lB20). The variance in bristle number attributable to the tuh-1 locus in nature is approximately 10.1%, an indication that the bristle phenotype is most likely a neutral, pleiotrophic side effect of tuh-1.

Analysis of the genes involved in organizing the tail segments of the Drosophila melanogaster embryo.

The metameric organization of the Drosophila melanogaster tail is obscured by developmental events that partially suppress or fuse some of its regions. To better define the developmental origins and segmental identities in the tail of the Drosophila embryo, we documented expression patterns and mutant phenotypes of several genes that play important roles in its morphogenesis. We documented the domains of engrailed (en), Abdominal-B (Abd-B) and caudal (cad) expression in the tail region. The staining pattern of cut (ct) was used to correlate the embryonic sense organs with their respective positions on the larval cuticle. The en patterns in different Bithorax-Complex (BX-C) Abd-B morphogenetic (m) and regulatory (r) mutants demonstrated that Abd-B functions to, among other things, suppress embryonic ventral epidermal structures on the posterior side of A8 to A9. Ventral epidermal structures were not added back into the en pattern in r- or BX-C- mutants, indicating that although the BX-C functions extend through A10, other non-BX-C genes must be required for development of this segment.

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

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.

Development of the D. melanogaster caudal segments involves suppression of the ventral regions of A8, A9 and A10.

Whereas the segmental organization of the thorax and anterior abdomen is morphologically delineated in both the Drosophila larva and adult, segments in the head and caudal regions lack such well-defined boundaries. Consequently, the organization of these regions has been difficult to decipher. In this study, transformations caused by the bithorax-complex homeotic mutants 48, M3, Ultraabdominal-1 (Uab1) and tumorous-head-3 (tuh-3), as well as the patterns of engrailed gene expression have been analyzed to investigate the segmental organization of the caudal segments. A special emphasis was placed on sense organs appearing in abdominal segments 8, 9 and 10 (A8-A10): We find that: (1) transformations in the caudal segments obey parasegmental borders; (2) the sense organs on A8, A9, and A10 are probably homologous to the pits and hairs in anterior A1-A7; (3) except for the larval anal tuft and the anterior side of A8, all structures in larval segments A8, A9 and A10 are dorsal/lateral in origin; and (4) dorsalization of embryonic A8 and A9 cells leaves space ventrally for A10, as it follows the contracting ventral nervous system during the embryological process of germ band contraction.

Paternal imprinting of inversion Uab1 causes homeotic transformations in Drosophila.

Paternal transmission of the bithorax-complex (BX-C) rearrangement, inversion Uab1, causes a specific dominant gain of function phenotype in most abdominal segments. This represents a case of paternal imprinting since the mutant phenotype will occur only if inversion Uab1 is paternally transmitted. The transformations in males are toward genital arch tissue. For females the transformations are to tissue found on abdominal segment 7 (Ab7) and to structures normally restricted to the genital disc. Ninety-six percent of transformed areas appear on Ab5 and Ab6 in both sexes and on Ab7 in females, coinciding with the Abd-B domain. Four percent of the transformations occurred on Ab1 through Ab4, coinciding with the abd-A domain. The mutant phenotype can be dramatically enhanced by modifying genes such as the posterior BX-C mutant tuh-3. Expressivity is modulated by maternal effect alleles interacting with tuh-3. A region of function within inversion Uab1 appears to be programmed during spermatogenesis to function in a legacy dependent manner during embryogenesis.

Tumorous-head-type mutants of the distal bithorax complex cause dominant gain and recessive loss of function in Drosophila melanogaster.

The homeotic mutants tuh-3, SGA62, I127, and R17.32 are located in the abdominal portion of the bithorax complex in Drosophila melanogaster. The genes act as semidominants in the head, causing a gain of expression of leg, genitalia, tergite, or combinations of the structures. SGA62, tuh-3, and I127 additionally act as recessives in the posterior abdomen, causing a loss of these functions. Each mutant has its own focus of expression in the head region. I127 and tuh-3 can cause head defects only in the presence of the recessive maternal effect allele tuh-1h, while SGA62 and R17.32 cause head defects in the absence of this maternal effect. In the presence of the dominant tuh-1g maternal effect allele, the tuh-3 and I127 heads are normal. However, these flies now show a genital disc defect. SGA62 homozygotes have abdominal segments 6 and 7 transformed into a more anterior segment irrespective of the maternal effect in force. R17.32 appears to map to the abd-A domain, while SGA62, I127, and tuh-3 belong to Abd-B. SGA62 is located in the morphogenetic element of Abd-B, while I127 has characteristics of mutants affecting both the morphogenetic and regulatory elements of Abd-B. The tuh-3 mutant is within the regulatory element. The maternal effect alleles appear to interact specifically with mutants in the regulatory region of Abd-B.