Q | Write a brief introduction to yourself including the lab you work in and your research background.
I am Kaustav Chakraborty, a postdoctoral researcher in Arnab Gupta's lab at the Indian Institutes of Science Education and Research, Kolkata, working with worms, specifically Caenorhabditis elegans. My PhD research focused on studying how intracellular copper [Cu(I)] contributes to neuronal and glial differentiation. Currently, I study how copper homeostasis contributes to reducing cadmium toxicity in C. elegans.
Q | How did you first get interested in science and/or your field of research?
My interest in biology began during my undergraduate studies in chemistry. Though the molecular structures were complex and challenging to memorize, their intricate design fascinated me and sparked my curiosity about their biological significance. This curiosity led me to pursue a master’s degree in biochemistry, where I delved deeper into the roles of molecules and ions within the body. I became especially intrigued by how even a single metal ion can trigger cascades of cellular reactions that determine cell fate. While an excess of these ions can be harmful, the precise regulation and interaction of signaling pathways captivated me. Understanding these intricate systems is key to unravelling how their disruption leads to metabolic diseases, many of which affect children. This could bridge the gap to translational research, contributing to potential treatments.
This drive led me to investigate the role of copper in neuronal and glial differentiation using both cell-based and animal models such as C. elegans. During my PhD, I studied them, amazed by how their behavior changes under various stresses and metal toxicities. I spent many hours observing their behavior under the microscope, trying to link neuro-molecular mechanisms to behavioral responses.
Q | Tell us about your favorite research project you’re working on.
The work I am undertaking holds special relevance in today’s world, as cadmium exposure has become a growing concern. Its major sources include cigarette smoking, soil erosion, and the consumption of crops cultivated on contaminated soil. Cadmium gradually accumulates in the human body, and with prolonged exposure it can cross the blood-brain barrier, accumulate in neurons, elevate reactive oxygen species (ROS), and eventually cause neuronal death.
Although researchers have explored the molecular mechanisms of cadmium toxicity, the distribution of cadmium across tissues and cell types, as well as its broader effects on the ionome and metallome, remain poorly understood.
To address these questions, I use the nematode C. elegans, a powerful multicellular model system, to investigate cadmium distribution and its effects on different cell types such as intestinal cells, neurons, and glia—cells that are also known targets of heavy metal toxicity in humans.
My current research specifically examines how excess cadmium disrupts neurotransmitter-based neuronal circuits and how these disruptions translate into altered behavior in worms. Furthermore, given that cadmium and copper share similar ionic properties, I am investigating whether genes involved in copper homeostasis contribute to cadmium detoxification and export it out from the cell.
Q | What do you find most exciting about your research project?
My best research experience represents a comprehensive effort to understand the mechanism of neurodegeneration linked to cellular copper homeostasis. My studies demonstrate a direct route of utilization of cytosolic copper towards the maintenance of neuronal viability and neurite generation in addition to its transport into the trans-Golgi network for incorporation into cuproproteins. Moreover, it emphasizes the importance of intracellular copper in neurite formation related to synaptogenesis. The cell-based model for differentiation may not fully mimic the in vivo conditions. I have employed C. elegans as a model organism to investigate the effects of the disruption of the cellular copper homeostasis. Deprivation of copper results in the degeneration of dopaminergic neurons in C. elegans.
Glial differentiation, on the other hand, is associated with low intracellular copper. Furthermore, the copper transporter residing at the glial neurite is shown to have role in neuronal copper supply. Nevertheless, this is the first systematic study to understand the complexities of copper utilization in two important cell types of the CNS. It sheds light on neurodegeneration associated with Menkes disease. The study emphasizes the importance of Cu(I) towards neuronal differentiation and communication between neurons and glia in maintaining copper balance in the CNS.
Q | If you could be a laboratory instrument, which one would you be and why?
I have always felt a special bond with the confocal microscope. In my PhD thesis, I even expressed gratitude to “Dr. Confocal Microscope” for guiding me through some of my most critical experiments. To me, the microscope is nothing short of magic. It transforms the unseen into the visible, allowing us to explore the hidden worlds within cells and organisms with stunning clarity.
As I move into my postdoctoral research, I cannot imagine a single experiment without some form of microscopy. My work lies in uncovering the molecular and cellular biology that shapes life, and in this pursuit, I aspire to become the microscope myself—a tool that helps others perceive the invisible, making the unseen seen.
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