Horticultural Sciences Department

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Research Overview

Research Overview | Projects & PublicationsUndergraduate Research | Course: PCB5065 - Advanced Genetics | Course: PCB6528

Mitochondria, the site of the TCA cycle, respiratory electron transfer and ATP synthesis, are essential to higher eukaryotic life. Mitochondrial function depends upon the coordinate action of mitochondrial and nuclear genomes. Our research is focused on the molecular-genetic dissection of mitochondrial biogenesis and function in higher organisms. This presents a challenge because mutations disrupting mitochondrial function are lethal in obligate aerobes. The cytoplasmic male sterility (CMS) systems of higher plants provide a solution to this dilemma. The mitochondrial genome encodes CMS, the maternally inherited failure to produce functional pollen. Nuclear fertility restoration genes block or compensate for the expression of CMS genes in the mitochondria, resulting in a male-fertile phenotype. We investigate molecular and genetic mechanisms of CMS and nuclear fertility restoration systems to understand how mitochondria effect cell death in plants and the ways in which nuclear genes influence the organization, inheritance and expression of mitochondrial genomes.
In addition to my work on mitochondrial biogenesis and function, I have been involved in a number of other projects that exploit techniques of plant molecular biology to facilitate plant improvement.


(a) Collapsed pollen of CMS-S maize exhibits morphological and molecular features of programmed cell death.  [photo by Dr. Lanying Wen] (b) Nuclear restorer-of-fertility mutations rescue the function of CMS-S pollen. These mutations are observed as sectors of male fertility on otherwise male-sterile plants. The mutation is recovered by using pollen from the sector to perform genetic crosses. [Photo by Dr. Susan Gabay-Laughnan] (c) Many restorer-of-fertility mutations are homozygous-lethal, leading to kernel abortion as seen on the bottom ear in panel c. The restorer-of-fertility lethal 1  (rfl1) locus functions in the biogenesis of mitochondrial ATP synthase, and kernels with rfl1/rfl1 embryos homozygous abort.  [Photo by Dr. Susan Gabay-Laughnan]