Abstract
We report on the generation and phenotype of mutant alleles of multiple edematous wings (mew), the gene encoding the αpsi subunit of the PS1 integrinof Drosophila. None of the six alleles examined makes detectable protein, and one allele results from a chromosome break near the middle of the translated sequence, so we are confident that we have described the null phenotype. In contrast to if (αPS2) and mys (βPS) mutants, most mutant mew embryos hatch, to die as larvae. Mutant mew embryos display abnormal gut morphogenesis but, unlike mys or if embryos, there is no evidence of defects in the somatic muscles. Thus, the complementary distributions of PSl (αPS1βPS) and PS2 (αPS2βPS) integrin on tendon cells and muscle, respectively, do not reflect equivalent requirements at the myotendinou junction. Dorsal herniation, characteristic of the mys lethal phenotype, is not observed in mew or in mew if embryos. Clonal analysis experiments indicate that eye morphogenesis is disrupted in mew clones, but if clones in the eye are relatively normal in morphology. Adult wings display blisters around large dorsal but not ventral mew clones. In contrast to dorsal mys clones, small mew patches do not necessarily display morphogenetic abnormalities. Thus, another integrin in addition to PS1 appears to function on the dorsal wing surface.
Original language | English (US) |
---|---|
Pages (from-to) | 1311-1320 |
Number of pages | 10 |
Journal | Development |
Volume | 121 |
Issue number | 5 |
State | Published - May 1995 |
Externally published | Yes |
Keywords
- Eye morphogenesis
- Mew
- Multiple edematous wings
- Muscle attachment
- PS integrin
- Wing morphogenesis
ASJC Scopus subject areas
- Molecular Biology
- Developmental Biology