Research Focus

Drosophila eye model to study axial patterning, cell survival & birth defects.

The fruit fly, Drosophila melanogaster, eye serves as an excellent model to study cell type specification during development. Drosophila eye has been extensively used to address diverse biological processes like patterning cell proliferation, cell death, cell survival, polarity and genetic basis of human diseases.  The compound eye of an adult fly develops from the primordium called eye imaginal disc harbored inside larva, which initiates from a group of 20- cells as early as an embryo.

The two major goals of my laboratory are: 

(I) Study the genetic basis of early eye patterning and growth with emphasis on axial patterning: Dorsal-Ventral patterning in Drosophila eye 

Axial patterning is hallmark of organogenesis which results in transition of a single sheet of cells into a 3-dimensional organ. Our lab is interested in understanding the molecular genetic basis of the Dorso-ventral patterning, the first lineage restriction event of early eye primordium. DV patterning thus plays a crucial role in inducing growth and patterning of early eye disc. The dorsal and ventral domains of the eye are generated by the domain specific expression and function of the dorsal selector genes and the ventral growth controlling genes. Our lab will focus on identifying new components of DV patterning and their role in retinal determination of the eye. Our laboratory seek to provide a better understanding of the molecular, genetic, and environmental basis of normal eye development, as well as elucidate the genes and molecules that when altered result in the genesis of birth defects in eye. 

(II) Discern mechanism of complex neuropathological disease, like Alzheimer’s Disease (AD). 

Alzheimer’s disease (AD), a common progressive neurodegenerative disorder in the aging population, has no early detection tests or proper cure. AD manifests as a gradual decline of cognitive functions of learning and memory due to selective atrophy of specific cell populations in central and peripheral nervous system. One of the causes of cytotoxicity seen in AD is generation and accumulation of amyloid-beta plaques in the brain. Even though produced in the body amyloid-ß42 (Aß42) is toxic and triggers neurodegeneration. The molecular genetic mechanisms that trigger progressive neurodegeneration due to Aß42 accumulation are not completely understood.

Several animal models have been developed to understand the molecular genetic, chemical basis of this disease. We are using a Drosophila eye model to understand the genetic circuitry involved in amyloid-beta 42 mediated neurodegeneration seen in Alzheimer’s disease.  Our long term goal to screen for (a) potential genetic mutations which contribute to/or trigger AD mediated neuropathology and may serve as biomarkers for early detection of AD and (b) potential drug targets which might either block the cellular process that leads to the accumulation of amyloid-plaques or which may prevent the oligomerization of Aß42 accumulation in the Drosophila eye.