Willow Pagon, Ummer Qureshi
Faculty Sponsor: Karen Hales
Mitochondria are energy harnessing organelles within the cell that have the ability to change shape. This phenomenon can be studied through Drosophila melanogaster spermatogenesis. Mutations in the protein Nmd have been linked to unusual mitochondrial phenotypes and male sterility. Msp1, an ortholog of Nmd in S. cerevisiae, has been shown to move from mitochondria to peroxisomes. Msp1 helps protect both mitochondria and peroxisomes from unwanted proteins. Nmd may have a similar role. Previous Hales lab members showed that when Nmd is not present, mitochondria are misshapen and peroxisomes do not form. Therefore, I hypothesize that Nmd also moves from mitochondria to peroxisomes which influences proper mitochondrial shaping and peroxisomal health. Further, nmd is an essential gene. Some alleles, however, only cause male sterility. The male sterile strain nmdp{ry4} exhibits unusual mitochondrial aggregation failure only in the testes. In this strain, a transposable P element is inserted in the 5′ untranslated region of the genome. We hypothesize that the P-element insertion in nmdp{ry4} males causes transcription to start from a cryptic promoter in somatic but not germline tissues. This results in sterility but not lethality. Initial reverse transcriptase quantitative polymerase chain reaction data indicate that mRNA levels in the testes of nmdp{ry4} males are significantly lower than mRNA levels in wild-type flies. mRNA levels in the heads of nmdp{ry4} males appear to be unaffected by the P-element insertion. These results support our hypothesis about the effect of the P-element insertion in nmdp{ry4} males, as well as our hypothesis about the overall function of Nmd.
