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S Tiong

Publications and source records attributed to S Tiong.

3 recordsLinked to original sources

msh specifies dorsal cell fate in the Drosophila wing.

Drosophila limbs develop from imaginal discs that are subdivided into compartments. Dorsal-ventral subdivision of the wing imaginal disc depends on apterous activity in dorsal cells. Apterous protein is expressed in dorsal cells and is responsible for (1) induction of a signaling center along the dorsal-ventral compartment boundary (2) establishment of a lineage restriction boundary between compartments and (3) specification of dorsal cell fate. Here, we report that the homeobox gene msh (muscle segment homeobox) acts downstream of apterous to confer dorsal identity in wing development.

Alleles↗

The Drosophila melanogaster ade5 gene encodes a bifunctional enzyme for two steps in the de novo purine synthesis pathway.

Steps 6 and 7 of de novo purine synthesis are performed by 5-aminoimidazole ribonucleotide carboxylase (AIRc) and 4-[(N-succinylamino)carbonyl]-5-aminoimidazole ribonucleotide synthetase (SAICARs), respectively. In vertebrates, a single gene encodes AIRc-SAICARs with domains homologous to Escherichia coli PurE and PurC. We have isolated an AIRc-SAICARs cDNA from Drosophila melanogaster via functional complementation with an E. coli purC purine auxotroph. This cDNA encodes AIRc yet is unable to complement an E. coli purE mutant, suggesting functional differences between Drosophila and E. coli AIRc. In vertebrates, the AIRc-SAICARs gene shares a promoter region with the gene encoding phosphoribosylamidotransferase, which performs the first step in de novo purine synthesis. In Drosophila, the AIRc-SAICARs gene maps to section 11B4-14 of the X chromosome, while the phosphoribosylamidotransferase gene (Prat) maps to chromosome 3; thus, the close linkage of these two genes is not conserved in flies. Three EMS-induced X-linked adenine auxotrophic mutations, ade4(1), ade5(1), and ade5(2), were isolated. Two gamma-radiation-induced (ade5(3) and ade5(4)) and three hybrid dysgenesis-induced (ade5(5), ade5(6), and ade5(8)) alleles were also isolated. Characterization of the auxotrophy and the finding that the hybrid dysgenesis-induced mutations all harbor P transposon sequences within the AIRc-SAICARs gene show that ade5 encodes AIRc-SAICARs.

Alleles↗

Recessive lethal mutations within the bithorax-complex in Drosophila.

Genetic deficiencies of the bithorax-complex (BX-C) in Drosophila, have been used to recover recessive lethal mutations in this chromosome region following mutagenesis. Complementation analysis separates these lethal mutations into five groups within a smaller deficiency, thought to remove the entire BX-C, and into 20 to the left and 4 to the right of the region. Homozygotes for each of only three groups of lethals, Ubx, abdA and AbdB, produce homoeotic segmental transformations in embryos. The functional domains of abdA and AbdB have been defined by changes in the appearance of larval hypodermal structures and of clones in imaginal tissue. The function abdA is required in all the compartments caudal to the anteroposterior border of abdominal segment 1 up to and including the anterior region of abdominal segment 8, whilst AbdB is required in abdominal segments 5 to 9. One allele of AbdB produces a ninth abdominal setal band and structures characteristic of head segments posterior to A8. Rare adult survivors hemizygous for an AbdB allele have eight abdominal segments in both sexes, and lack genitalia in females. Our findings are discussed in the context of the organisation of genetic functions within the BX-C.

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