Research Groups

Current Lab Members

Name Position Email Phone
Adhikary, Babli Guest
Ahmed, Salma Predoc +49 351 210-2921
Dye, Natalie Acting RGL +49 351 210-2806
Fuhrmann, Jana Predoc +49 351 210-2683
Ghosh, Suhrid Sundar Predoc +49 351 210-2593
Iyer, K. Venkatesan Postdoc +49 351 210-2814
Jahagirdar, Sanika Guest student
Krishna, Abhijeet Predoc +49 351 210-2643
Mahmoud, Ali Technician +49 351 210-2575
Nellas, Ioannis Predoc +49 351 210-2574
Piscitello Gómez, Romina Ph.D. Student +49 351 210-2931
Thepkaysone, May-Linn Technician

Morphogen and hormonal signaling:


For my PhD, I am working on metabolism and morphogen signaling pathways. During the last few years, the sequence of mechanical and molecular events during morphogenesis has been extensively studied. However, little is known about the metabolic events that support growth and differentiation. The imaginal wing disc of Drosophila is an excellent model tissue for genetic manipulations. Using this highly proliferative tissue, I am questioning the state of cell energy metabolism during growth. To answer this question, I am using biochemical and advanced biophysical tools to explore and visualize the wing disc’s metabolism and investigate the signaling molecules that influence it.


I am interested in studying inter-organ signaling and resource allocation during growth and development. In my current project, I am trying to understand how Drosophila insulin-like peptides coordinate tissue growth during larval development. My research shows that insulin, a hormone primarily regulated by nutrition, may be involved in supporting growth in the absence of food during the late larval stages. Additionally, the starvation pool of insulin might be directly regulating the production of ecdysone, the molting hormone, in a non-canonical fashion involving a neuronal relay mechanism.


The Eaton lab has worked for several years on Sonic hedgehog signaling (Shh) in mammalian cells, discovering how the morphogen is released when lipid associated. It is intriguing how one ligand fine tunes the signaling amplitude in diverse contexts via the primary cilium. In the last decades, research efforts have documented the existence of lipid modifications on the Shh ligand. Yet, the molecular mechanism by which Shh lipid modifications influence signaling amplitude remain poorly understood. During my PhD, I am studying how these modifications modulate signaling through the dynamics of Shh pathway components in the cilium. I answer this question using quantitative imaging and biochemical tools. Recently, I moved to the Tabler lab, where I will continue to apply molecular-level approaches to determine the role of Shh lipid modifications on signaling and tissue biology.


Sonic hedgehog (Shh) is a key regulator of homeostasis in many adult tissues and drives proliferation in different cancers, including some adrenal carcinomas. It is still unclear, however, what regulates the Shh pathway activity in the adrenal cortex and how this pathway becomes upregulated in adrenocortical carcinoma. Therefore, I am studying the modes of secretion of the Shh protein and the range and specificity of pathway activation in the adrenal cortex using adult mouse adrenal glands and a human adrenocortical cancer cell line. I am employing biochemical methods to characterize the Shh protein form and secretion mechanisms, immunofluorescence to localize the Shh pathway components in mouse adrenal glands and cell-based assays, and gene expression to study Shh pathway activity in responding cells.

Cell/Tissue mechanics:


How is collective cell behavior orchestrated during development? During my PhD I am addressing this question using the pupal wing of the fruit fly as a model system. The pupal wing undergoes a dramatic morphogenetic remodeling that gives rise to the tissue shape, but it remains unclear which molecular mechanisms determine the tissue mechanical properties during tissue flows. Combining physical and biological approaches, I am investigating the relationship between stress and strain in both wild-type tissues and a variety of planar cell polarity mutants. Overall, my work aims at bridging the molecular, cellular and tissue scales to understand the robustness behind tissue morphogenesis.


The aim of my PhD project is to understand how individual cell behaviors collectively transform the shape of epithelial tissues in three dimensions. I am addressing this question on the eversion of the Drosophila wing imaginal disc, which is undergoing a transition from a folded epithelial monolayer to a flat, bi-layered epithelium. I am using a combination of light-sheet and confocal imaging and image analysis to address how cellular rearrangements and tissue scale patterns of cell packing geometry affect complex and dynamic changes in tissue architecture. My eventual goal is to develop a physical model describing these observations to generate novel insight into 3D shape changes in epithelial tissues.


The mechanisms by which tissue surfaces develop to form complex 3D morphologies is an interesting question from the perspective of developmental biology. One of the simplest cases of shape change in tissues is going from a flat sheet to a dome shaped structure. We are interested in studying this shape change in two different systems. The first system is wing disc pouch which shows similar shape change during development. We want to quantify the planar deformation using live microscopy data. Using this data, we perform simulations to show that such a pattern of planar deformation can bring change in the 3D shape of the tissue. The second system is human induced pluripotent stem cells which can be differentiated into intestinal epithelial cells. These cells then self-organize to grow spheroids which bud off and float in the media. We are interested in describing and understanding this change in the 3D shape of the culture.


How tissue mechanics influences nuclear mechanics is an intriguing question in epithelial biology. Nuclear mechanics is regulated primarily by nuclear scaffold proteins – Lamins. My research is focused on understanding how epithelial tissue mechanics influences Lamin A/C levels. Using Drosophila epithelial tissues and MDCK cell monolayers, as a model system, I have revealed that Lamin A/C scales with apico-basal cell compression. Using genetic perturbations in the Drosophila wing disc, I revealed that apico-basal compression regulates Lamin A/C levels. I have also developed a MDCK monolayer based system to investigate how apico-basal compression deforms the nucleus and induces Lamin A/C expression. The new mechanism for Lamin A/C regulation in epithelial tissues that I have identified give new insights into the interplay between nuclear mechanics, tissue mechanics and mechanotransduction in development and disease.

General Contact Information

Max Planck Institute
of Molecular Cell Biology and Genetics
- Dye / Eaton -

Pfotenhauerstr. 108
01307 Dresden

Phone +49 351 210-2501
Fax +49 351 210-1309