mitosis & nuclear chromosome
slsj1D7 heterozygotes also heterozygous for either cherEPSΔ5 or chersko, but not cherQ1042X, exhibit flight defects, since high frequency wing beat is only sustained for a few seconds, as compared to wild-type and single heterozygous controls; in both genetic background, however, there are no obvious sarcomere defects.
Heterozygosity for slsj1D7 enhances the semi-lethality and the myofibril shredding defects (even leading to the loss of the sarcomere structure) resulting from the expression of cherJF02077 under the control of Scer\GAL4Mef2.PU.
Pupae trans-heterozygous for tnMJO-348 and slsj1D7 undergo proper pupal morphogenesis and eclosion. Notably, mutant pupae homozygous for tnMJO-348 and heterozygous for slsj1D7 are slim and show a statistically significant increase in length when compared to homozygous tnMJO-348 pupae. This result indicates a suppression of the muscle contraction and morphogenetic defects that are associated with the tnMJO-348 mutant phenotype.
slsj1D7 heterozygosity greatly increases the adult lethality of Df(3R)Mlp84BP8/Df(3R)dsx2M mutants. slsj1D7 heterozygosity also exacerbates the pupal case elongation phenotype associated with Df(3R)Mlp84BP8/Df(3R)dsx2M or Mlp84BP20/Df(3R)dsx2M.
slsj1D7 heterozygosity in a Df(3R)Mlp84BP8/Df(3R)dsx2M mutant background leads to striking muscle abnormalities. Most muscle fibers are wavy and/or spindly in appearance. A significant number of fibers are torn or show some degree of fraying. Closer examination of the double mutants reveals a profound loss of sarcomeric structure of single muscle fibers from third instar fillet preparations. Neither Df(3R)Mlp84BP8/Df(3R)dsx2M hemizygotes, nor slsj1D7 heterozygotes on their own display any obvious structural abnormalities at the light microscopic level.
L. and Y. Jan.