Authors: Rachel Cathey, Karen Chasmusco, Christine Chase
Faculty Mentor: Christine Chase
College: College of Agricultural and Life Sciences
In cytoplasmic male sterility type S (CMS-S) maize, expression of a mitochondrial CMS gene causes pollen cell death. We hypothesize that loss-of-function mutations in nuclear genes normally required for mitochondrial gene expression will rescue CMS-S pollen. Nuclear genome mutations with the ability to thwart CMS-S were sought through a reverse genetics screen for restorer-of-fertility (restorer) mutations. The mutations selected were Mutator (Mu) transposon insertions in mterf, rpl27, and oxa1 genes, introduced through cross pollination onto CMS-S plants. Pollen-fertile progeny were recovered and the mutations were followed by PCR through a back-cross pollination to CMS-S plants. If the mutations are restorers, the hypothesis predicts all back-cross progeny plants will inherit the mutation and be pollen-fertile. We demonstrated the presence of the candidate restorer mutations in the progeny. Using Chi-squared analysis, p-values of less than 0.001 for both rpl27 and mterf and between 0.01 and 0.001 for oxa1, demonstrated strong genetic linkage between our mutants and fertility restoration. Each family did, however, include a few exceptional plants that did not carry the candidate restorer. Future plans are to look towards the cause of the exceptional plants, to see if there are additional unknown mutants contributing to the restoration of pollen function.