The interviews for PhD admission at the Department of Developmental Biology and Genetics will be held in May 2026. The time and venue for your interview have been provided in the call letter issued by IISc.
Please make it convenient to appear for the interviews if shortlisted.
Please bring the following documents for the interviews:
1. IISc issued interview letter.
2. Government-issued ID card.
3. Mark sheets for 10th, 12th, Graduate and Post-Graduate courses.
4. National entrance test certificate/score card.
Please follow the guidelines as per the interview call letter and email sent by DBG interview coordinators.
Interview results will be announced on the following link https://dbg.iisc.ac.in/phd-interviews-2026/
Dear Candidates,
We welcome you to the Interview at the Department of Development Biology and Genetics (DBG) at IISc.
The interview will be conducted offline, in person at DBG.
You will be interviewed for approximately 15-20 minutes
INSTRUCTIONS TO CANDIDATES
Please look for signboards and instructions in the main lobby of the Biological Sciences Building.
You should reach the DBG seminar hall and sign the attendance sheet on the date of your interview (at the assigned time as per the interview call letter). DBG Seminar hall is located on the 1st floor. You will be assigned to the interview committees. The office staff will guide you to the room where the interviews will be held.
You can write to office.dbg@iisc.ac.in for more details.
Candidates must collect the “Faculty Preference Form” from the DBG Office and submit it to the DBG Office before the end of the day of their interview.
Should you need any further information, kindly contact the DBG office (office.dbg@iisc.ac.in).
For further information, please also visit faculty home pages.
All the best,
Chair, DBG. IISC
Lab research topic: Cancer Stem Cells
Stress-adaptations in circulating cancer stem cells: targeting metastatic vulnerabilities
Circulating tumor stem cells must endure the hostile conditions of the bloodstream in order to successfully seed metastasis. During this journey, they encounter multiple stresses, including shear forces, physical constriction within capillaries, immune surveillance, and ‘anoikis’ – cell death triggerred by loss of matrix-attachment. In order to survive, cancer cells undergo adaptive cellular reprogramming enabling them to shift to a stem-like state and acquire drug resistance. Previous work from the laboratory has identified a critical role for the energy sensor kinase AMPK in promoting survival under matrix-deprivation stress by restoring energy balance through suppression of anabolic processes and activation of catabolic pathways.
Protein translation is a major energy-consuming anabolic process which is tightly regulated under stress. Prior findings from the lab reveal that matrix-detached cancer cells suppress global protein synthesis while selectively enhancing translation of specific RNA subsets. Building on this, the proposed project aims to elucidate stress-induced rewiring of cellular metabolism, as well as transcriptomic and translatomic landscapes. Using integrative approaches such as mass spectrometry, polysome profiling, and RNA sequencing, this study seeks to identify novel molecular targets to curb metastasis.
References:
The project will involve investigations into signaling systems in mycobacterial systems or aging cells / organisms using multiomics approaches and identify regulatory nodes that can be used for therapeutic targeting. The student will make use of molecular, cellular, omics, data sciences and systems biology approaches.
Check more details on the website – https://sites.google.com/site/sainislab/home
The synthesis of proteins using genetic information and its regulation is a fundamental process in all life forms. These processes play an important role in many key life processes including early embryonic development, learning and memory as well as in response to cellular stress. Although translation initiation is a fundamental and indispensable process, many of its aspects are poorly understood. We employ biochemical, mutational and structural biology approaches to understand the molecular details of the initial steps of protein synthesis and to figure out how it is regulated (see recent publications). This is essential for developing novel therapeutic strategies for many human disorders/ cancers and against bacterial, fungal and viral infection.
Bacterial translation initiation requires three initiation factors IF1, IF2 and IF3 which cooperatively bind to the small ribosomal subunit (30S) and positions the initiator tRNA (fMet-tRNAfMet) over an mRNA with an appropriate translation initiation region (TIR). For efficient protein synthesis, many bacterial mRNAs contain a purine-rich Shine-Dalgarno (SD) sequence (4-9 nucleotides in Escherichia coli) upstream of the start codon having base complementarity to anti-SD (aSD) sequence at the 3’end of 16S rRNA. The 30S subunit, along with the IFs and fMet-tRNAfMet, form an unstable 30S pre-initiation complex (PIC) initially.
Although bacterial translation initiation is much simpler, we do not have a detailed mechanistic understanding of the entire pathway. The incoming PhD student would build up on this ongoing project to understand the molecular details of bacterial ribosomal pre-initiation complexes using molecular biology, biochemistry, and structural biology techniques.
For further details of the project, contact Prof. Tanweer Hussain (Lab: GB-04; Email: hussain@iisc.ac.in)
To be updated
To be updated
Our lab studies host-microbiome interactions. We use diverse multi-omic approaches including genomics and metagenomics, to elucidate the impact of the microbiome on host nutritional physiology, development, reproduction, behaviour and function. Our primary focus is on insects – an extraordinarily successful group of organisms that show complex and intricate associations with microorganisms. We aim to leverage insect-microbiome interactions to develop novel biotechnological applications in health and agriculture. Using whole genome sequencing, metagenomics, transcriptomics, metabolomics, microscopy, and by combining approaches in molecular biology, biochemistry, ecology, and evolution, we study the role of microbiota in host adaptation.
Control of glucose homeostasis due to pancreatic paracrine secretions.
Our lab investigates how pancreatic β‑cells sense glucose and translate it into precise insulin secretion, with a focus on metabolic signalling microdomains and GLUT trafficking. We recently showed that GLUT1/2 dynamically traffic to the plasma membrane at high glucose, creating local Ca²⁺ microdomains that act as a metabolic switch coupling glucose uptake to exocytosis. Disruption of GLUT regulation in type 2 diabetes reduces β‑cell responsiveness and destabilises glucose homeostasis (Pallavi, et al, PNAS, 2025). This work connects metabolic sensing, signalling microdomains, and insulin exocytosis in a unified framework, positioning glucose transport not just as nutrient entry but as an active regulator of β‑cell function.
Our lab uses the same single-granule, live-cell imaging approach we developed for β‑cells to study α‑cells (glucagon) and δ‑cells (somatostatin), revealing how paracrine signalling within the islet is disrupted in type 2 diabetes (Gandasi, et al, Diabetologia, 2023 and 2024). In this project PhD student will apply the same toolkit: TIRF microscopy, single-vesicle tracking, GLUT trafficking studies, and signalling perturbations to α‑ and δ‑cells. The idea is to understand how metabolic sensing and mechanisms jointly control glucagon and somatostatin secretion to maintain glucose homeostasis in a paracrine manner.
Unravelling Exocrine-Endocrine Interactions in Pancreatic Disorders
The pancreas is a vital organ in the digestive system with a unique dual functionality where it behaves both as an exocrine and endocrine gland, which plays an important role in aiding digestion and maintaining blood glucose homeostasis, respectively. Pancreatitis is a complex, progressive inflammatory syndrome of the predominantly exocrine part of the pancreas. In adult-onset chronic pancreatitis, the pancreatic lobes are severely compromised, which we document from the Indian population as well. Paediatric pancreatitis, although rare, has an increasing burden globally. Paediatric pancreatitis mostly has a genetic aetiology, unlike pancreatitis in adults, which can be due to alcohol consumption, gallstones, etc. Various studies across the globe have reported some genetic risk factors in different paediatric populations. The most documented risk genes are SPINK1, PRSS1, and CFTR. There are no documented risk genes in the Indian population. To address the problem, we will collect peripheral blood samples from paediatric pancreatitis patients and sequence the whole exome. The identified mutations in risk genes would be a great tool for early identification and treatment of paediatric pancreatitis. Further, we will test these variants on the release of exocrine hormones to create a model to screen for anti-inflammatory drugs to treat paediatric pancreatitis. In addition to genetic risk variants, we will investigate the role of microRNAs in disease pathology and early diagnositc marker.
Admission to the department for this degree is through a division wide selection process which involves qualifying a written test followed by a interview process.