My research program is focused on understanding the genome level determinants of the diversification between evolutionary lineages. The approach that I use towards this end is computationally based and consists of the comparative analysis of large-scale genomic sequence, expression and functional data sets. This approach is facilitated by the accumulation of genome-scale data sets and the continuing development of the computational applications and infrastructure needed to exploit such data. Ultimately, I hope to integrate our understanding of how evolutionary forces play out at distinct levels of biological organization. More specifically, I am interested in understanding the nature of evolutionary innovations that have led to the emergence of complexity in eukaryotic lineages. I currently explore three distinct research areas relating to the evolution of eukaryotic genome complexity: i-the contributions of transposable elements to host gene regulatory and protein coding sequences, ii-the tempo and mode of gene regulatory and expression divergence and iii-convergent evolution of gene function
Physiological and biomechanical mechanisms underlying fine motor skills and their adjustments and adaptations to heightened sympathetic nerve activity, aging or inactivity, space flight or microgravity, neuromuscular fatigue, divided attention, and practice in humans. He uses state-of-the-art techniques in neuroscience, physiology, and biomechanics (e.g., TMS, EEG, fMRI, single motor unit recordings, microneurography, mechanomyography, ultrasound elastography, and exoskeleton robot) in identifying these mechanisms.
Our research focuses on the host-pathogen relationship and uses 1) host genetic studies of infectious diseases (tuberculosis, leprosy, Buruli ulcer) and 2) molecular systems biology studies of nano-vesicular exosomes released from stimulated immune subsets.
Cardiac and skeletal muscle excitation-contraction coupling;regulation of ryanodine receptor calcium release channels by endogenous effectors; single channel electrophysiology; muscle aging, fatigue and disease.
We are interested in understanding the genetic basis of heritable behavioral variation. In the current age, it has become cheap and easy to catalog the set of genetic differences between two individuals. But which genetic differences are responsible for generating differences in innate behaviors, including liability to neurological diseases such as autism, bipolar disease, and schizophrenia? How do these causative genetic variants modify a nervous system? Besides their role in disease, genetic variation is the substrate for natural selection. To understand how behavior evolves, we must understand how it varies.