Chloroplast biogenesis is a complex developmental process that entails the conversion proplastids found in leaf meristems or etioplasts from dark grown seedlings, into fully functional, mature chloroplasts. Variegation mutants are excellent tools using which one can gain access into the poorly understood mechanisms governing chloroplast biogenesis.

The Rodermel lab has been interested in characterizing the immutans (im) variegation mutant of Arabidopsis, one of the best-characterized chloroplast biogenesis mutants that defines the gene for the Plastid Terminal Oxidase (PTOX). Over the years, we have focused our efforts in identifying second-site genetic suppressors of immutans to obtain mutants that can rescue the variegation phenotype in the im background by either replacing or bypassing the need for PTOX.

My research work in the Rodermel lab has been primarily focused on the characterization of bypass suppressors of immutans. Two new bypass suppressors of immutans have been identified - gigantea and ef1A, both of which offer distinct photosynthetic compensatory mechanisms by which they rescue the variegation phenotype associated with immutans. gigantea suppresses variegation in immutans phenotype of immutans during the late stages of plant development through a complex signal transduction pathway involving crosstalk with hormones like cytokinins and GA. ef1A, instead, functions to delay chloroplast biogenesis in im and hence rescues variegation in the im background. Suppression of the plastid defect in both imgi and imef1A is likely caused by a relaxation of excitation pressures in developing plastids by factors contributed either directly or indirectly by gi and ef1A.

Extending from my work on characterizing mechanisms regulating chloroplast biogenesis, I have also functionally characterized the first bona fide Arabidopsis chloroplast genome encoded antisense short ORF that plays an important role in regulating RNA processing events within the chloroplast genome.