Developmental studies on two ecdysone deficient mutants ofDrosophila melanogaster

Abstract

This paper describes two ecdysone-deficient, recessive-lethal mutants,lethal(1)giant ring gland (grg) andlethal(1)suppressor of forked (mad-ts: Jürgens and Gateff 1979) and compares their ecdysteroid titers with that of the wild-type. Mutant larvae show a much reduced ecdysteroid content, amounting to 1/10 to 1/30 of the wild-type values, but never a true titer peak. They fail to pupate and die after 1-3 weeks. Ecdysteroid feeding elicits different responses in the larvae of the two mutants.mad-ts larvae pupate within 24 h, thus showing that their low ecdysteroid titer is directly connected to their inability to pupate.mad-ts resembles the mutantlethal (3)ecdysone-1 (Garen et al. 1977). Thegrg mutant larvae, on the other hand, fail to pupate after 20-hydroxyecdysone feeding as well as injection. The primary defect of thegrg mutant is not entirely clear. Thegrg larval salivary gland cells appear to possess normal ecdysteroid receptors. Furthermore, the low ecdysteroid titer ingrg is not the result of an increased ecdysteroid catabolism. The primary defect in the mutant may lie in the malfunctioning neurosecretory cells which do not show neurosecretion in histological preparations. Further support for this notion comes from electronmicrographs of the enlargedgrg ring glands which, in contrast to the wild-type, do not possess nerve endings.In the wild-type three ecdysteroid peaks were found: one shortly before puparium formation, the second at approximately 12 h and the third at about 30 h after pupation. The ecdysteroid titer peak in late third instar, wild-type larvae is mainly due to the presence of 20-dydroxyecdysone as shown by radioimmunoassays after thin layer chromatography and derivatization followed by gas liquid chromatography and mass spectroscopy. In addition, a number of unidentified polar and apolar metabolites were also present.

Smt3 is required forDrosophila melanogastermetamorphosis

“…However, the nucleus is affected in smt3i PGs, showing an abnormal morphology, thickening of the nuclear lamina and hyper-proliferation of VLPs. A similar increase in the amount of VLPs has been found in at least one other ecdysteroid mutant, grg (Klose et al, 1980). smt3i PG nuclei also showed arrays of parallel electron-dense stripes, a phenotype that increased gradually during the prolonged larval life.…”

“…The hypertrophy of PG cells and their nuclei found in smt3i larvae has also been reported in ecdysteroid deficient mutants, such as mld, woc, grg or dre4 (Klose et al, 1980;Neubueser et al, 2005;Sliter and Gilbert, 1992;Wismar et al, 2000). This could reflect a compensatory mechanism triggered by the abnormally low ecdysteroid levels common for all these genotypes.…”

“…Woc controls the conversion from cholesterol to 7dC, Mld is involved in the regulation of spok, and βFtz-f1 is involved in the transcriptional regulation of dib and phm (Ono et al, 2006;Parvy et al, 2005;Warren et al, 2001). Several other genes in Drosophila are implicated in the control of ecdysone titers, such as ecdysoneless (ecd) (Henrich et al, 1987), giant ring gland (grg) (Klose et al, 1980), dare (Freeman et al, 1999), giant (Schwartz et al, 1984), dre4 (Sliter and Gilbert, 1992) or the inositol 1,4,5,-tris-phosphate receptor (Venkatesh and Hasan, 1997), although for most of them their mechanism of participation in steroidogenesis is unclear.…”

The timing of Drosophila salivary gland apoptosis displays an l(2)gl-dose response

“…49 Moreover, salivary gland underdevelopment occurs before the outgrowth of the tumours and, thus, can be directly attributed to the absence of l(2)gl gene activity in these tissues, further supporting the idea that ecdysone deficiency alone is not sufficient to cause neoplastic growth. 50,51 Although p127 is expressed at a relatively high level in wild-type salivary glands, 3 no major dramatic abnormality could be observed in the salivary glands with the exception of a smaller than normal size 41 and a reduced degree of chromosomal polytenization, 42 suggesting that p127 functions differently in this tissue than in brain and imaginal discs. Investigations on the role played by p127 in the salivary glands may thus be highly informative to understand the pleiotropy of its cellular functions and will help to unravel new and unsuspected activities of l(2)gl during Drosophila development.…”

Variation in the amount and activity of esterase 6 in a natural population of Drosophila melanogaster

“…The elimination of X-effects in the present study also suggests that the variation we detected was not mediated by differences in juvenile hormone or ecdysone titres. Both hormones induce EST6 activity in isolated male abdomens (Richmond and Tepper, 1983) and the X is the only chromosome to which factors affecting the titres of these hormones have been mapped (Kiss et a!., 1978;Klose et a!., 1980). Although much of the activity variation was thus likely to be inherited on the (third) chromosome containing the EST6 locus, very little of the variation was associated with the structural variants of this locus detected by electrophoresis.…”