Amrita Jain


Name: Amrita Jain
Nationality: Indian

Dept. Molecular Cell Biology,
Fachbereich Biologie/Chemie,
University of Osnabrueck
Barbarastrasse 13,
49076 Osnabrueck,

Contact details: T: +49 541 969 7222
F: +49 541 969 2884
M: 017676826897
E mail: Amrita.Jain@Biologie.Uni-Osnabrueck.DE


Amrita has Indian nationality. She completed her Bachelor’s degree in Biotechnology from Devi Ahilya University India and earned the Master’s degree in Genomics from Madurai Kamaraj University, India in year 2011. She then spent a year as research assistance in the laboratory of Dr. Pushkar Sharma at the National Institute of Immunology, New Delhi working on the characterization of novel signaling pathways in neuronal apoptosis. Recently, she had joined her D.Phil degree at University of Osnabrueck under supervision of Prof. Dr. Joost Holthuis. Her scientific interest lies in study of ceramide homeostasis machinery involved in cell apoptosis.

In addition to Cell biology and Molecular genetics, Amrita has acquired experience in virology and metagenomics and toxicology. Her technical expertise includes molecular biology, tissue culture and fluorescence microscopy amongst other.

Amrita Jain is primarily based at the university of Osnabrueck ( but will spend a part of her  fellowship in the laboratory of Dr. Carsten Schultz at European Molecular Biology Laboratory, Heidelberg. to learn Bi-functional lipid technology.  Her Sphingonet project is entitled as “Manipulation of Biosynthetic ceramide flows and its impact on cell fate and organization”

Project title: Manipulation of biosynthetic ceramide flows and its impact on cell fate and organization

Project summary:

Ceramides are central intermediates of sphingolipid metabolism with critical functions in cell organization and survival. They are synthesized on the cytosolic surface of the endoplasmic reticulum (ER) and then transported by ceramide transfer protein CERT to the Golgi for conversion to sphingomyelin (SM) by SM synthase SMS1. We previously identified SMS1-related protein SMSr as a critical regulator of ceramide levels in the ER. Disruption of SMSr function causes a rise in ER ceramides and their mistargeting to mitochondria, triggering mitochondrial apoptosis. How ER ceramides reach mitochondria is not known. Their delivery may rely on intimate membrane contacts between the two organelles, a cytosolic transfer protein acting at the ER-mitochondrial interface, or both.

To explore the molecular principles by which ER ceramides are delivered to mitochondria, we here use constitutive and drug-inducible tethers that allow a manipulation of contact surface area and gap-width at ER-mitochondria junctions. In addition, we engineered CERT proteins to redirect the biosynthetic ceramide flow from the Golgi to mitochondria and will investigate their impact on cell fate and organization. As a complementary approach, we use photo-activatable and clickable ceramide analogues to trace ceramide trafficking machinery at the ER – mitochondria interface.

This project is supervised by Prof Dr. Joost Holthuis ( and performed by Amrita Jain at the University of Osnabrueck, Germany.


Joost Holthuis (University of Osnabrueck, Germany)
Carsten Schultz (European Molecular Biology Laboratory, Heidelberg)

Biosketch 1st scientific supervisor:

Joost Holthuis studied biology at Utrecht University, NL, and graduated with honors on neuroendocrine secretion in 1996 at the Radboud University Nijmegen, NL. Following postdoctoral studies on syntaxins with Hugh Pelham at the MRC Laboratory of Molecular Biology in Cambridge, UK, he returned to the NL to start his own group at the Academic Medical Center in Amsterdam. In 2001 his group moved to the Bijvoet Center and Institute of Biomembranes at Utrecht University, where he worked as associate professor. In 2012 he accepted a position as professor of Molecular Cell Biology at the University of Osnabrueck. Research in his group focuses on membrane lipid metabolism, transport and homeostasis; the underlying protein machinery of lipid converters, sensors and flippases; and how dysfunction of this machinery results in systemic failure and disease.