Welcome to the Singh Lab, where we explore the genetic and molecular mechanisms underlying eye development and neurodegeneration, using Drosophila melanogaster (fruit fly) as a model system. Our research spans two major areas:
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 development of a fully functional eye begins with a single sheet of epithelial cells and transforms into a complex, three-dimensional organ. Our lab investigates how axial patterning, particularly along the dorsal-ventral (DV) axis, shapes this transformation during the early stages of Drosophila eye development.
We study how dorsal selector genes and ventral growth-regulating factors establish distinct tissue domains and coordinate the initial lineage restriction events that drive retinal development. By using genetic tools, molecular assays, and advanced microscopy, we aim to:
Identify new genes and pathways involved in DV axis specification
Understand how DV patterning controls growth and retinal determination
Explore how disruptions in these processes contribute to congenital eye disorders
This research provides critical insight into how organ patterning and morphogenesis are genetically programmed—and how similar mechanisms may be disrupted in human birth defects affecting the eye.
In addition to developmental genetics, our lab studies neurodegenerative diseases, with a particular focus on Alzheimer’s disease (AD). Using a Drosophila eye model, we express the human amyloid-beta 42 (Aβ42) peptide to investigate how it induces cellular toxicity, neural atrophy, and retinal degeneration—phenotypes that closely mimic key aspects of AD.
Our goals in this research area are to:
Discover genetic mutations and modifiers that enhance or suppress Aβ42 toxicity
Uncover the molecular pathways involved in Aβ42 aggregation and neuron death
Identify potential biomarkers for early detection
Contribute to the development of novel therapeutic targets for AD
By leveraging the genetic power and speed of discovery in Drosophila, our lab provides valuable insights into the complex biological processes behind neurodegeneration—insights that can inform and accelerate translational research in mammalian systems.
The lab’s long-term goals are to (a) identify genetic mutations that contribute to or trigger AD-related neuropathology, which could serve as biomarkers for early detection, and (b) discover potential drug targets that could block the cellular processes leading to amyloid plaque accumulation or prevent the oligomerization of Aß42.