My research interests are in the broad areas of Sexual conflict, Sexual Selection, Life-History Evolution and Evolutionary Ecology of Immunity. My research program aims to understand the effects of sexual conflict and sexual selection on aging and immune response. Theory predicts that intersexual conflict promotes increased investment in sexual activity under certain conditions. Hence, when these conditions are satisfied, increased investment in reproduction related activity should divert resources away from other activities involved with somatic maintenance. Further, sexual conflict may also influence the sex- specific gene regulation, especially of the ones involved in metabolic and immune path ways. Hence iIt follows that with resource acquisition having an upper limit, sexual conflict will influence both aging and immunity. I am testing these hypotheses using classical laboratory selection, phenotypic manipulation as well as molecular approaches.
During my post-doctoral work, I explored the role of intralocus conflict in maintaining genetic variation in fitness. Intralocus conflict arises because the sexes share the same gene pool, with expression of the same alleles having opposite effects on relative fitness in each sex. This form of sexual conflict evolution resembles a tug-of-war over gene expression in which each sex is prevented from evolving towards its optimal phenotype by the genetic correlation between them (Rice and Chippindale 2001), thereby reducing the average fitness of each sex leading to a gender load.
Even though previous studies have documented the existence of sexually antagonistic variation, the evidence for the evolutionary importance of gender load is not clear. Moreover, the traits involved in intralocus conflict and consequently the underlying mechanisms have not been investigated. I tested this hypothesis by creating replicate populations of Drosophila in which gene expression is limited to males, thus setting them free from female- specific selection pressures. These male-limited genomes have rapidly evolved higher fitness when expressed in males and lower fitness when expressed in females. Additionally a host of sexually dimorphic traits have moved closer to a male-specific optimum, clearly indicating a role for intralocus conflict in maintaining genetic variation in fitness.
During my doctoral research, using Drosophila melanogaster as the model system, I studied the role of trade-offs in maintaining genetic variation in pre-adult development time, a trait extremely important for fitness. sUsing laboratory evolution, I successfully selected replicate populations of D. melanogaster for faster pre-adult development and early reproduction for nearly 200 generations, with the selected populations developing nearly 25% faster than their controls and thereby demonstrated the existence of genetic variation in this trait. I discovered a host of trade-offs surrounding development time that could help maintain the genetic variation in this trait. I have also shown that selection for faster development can decrease adult stress resistance, lipid and glycogen storage and affect aging in a complicated manner through a physiological resource allocation switch. I have looked at the implications of life history evolution to dynamics of populations and provided the first empirical evidence that population stability can evolve as a by product of selection on faster pre-adult development - a trait that is not directly related to any of the stability determining parameters.