Inhalt
In 2009, I graduated from ICFAITech (ICFAI University, Hyderabad, India) with a B.Tech. in Biotechnology. I completed my Bachelor's thesis from The University of Western Australia, Perth, Australia. In 2011, I graduated from BITS (Birla Institute of Technology & Science, Pilani, India) with a M.E. in Biotechnology. My Master's thesis was accomplished at The Centre for DNA Fingerprinting and Diagnostics, Hyderabad, India.
During the IGSDHD rotation period, I worked on the following projects:
- Lab of Prof. Dr. Angelika Noegel, Institute for Biochemistry I, Medical Faculty, University of Cologne: "Role of CRN5 in MAPK14 signaling pathway"
- Lab of Dr. Tina Wenz, Institute for Genetics, University of Cologne: "Effect of PTF on mitochondrial function"
- Lab of Prof. Dr. Jonathan Howard, Institute for Genetics, University of Cologne: "Characterization of an "atypical" Toxoplasma gondii isolate from Brazil (South America)"
Since March 2012, I have been working on my PhD project in the Lab of Prof. Dr. Angelika Noegel.
Characterization of a Coronin 7 (CRN7) knock-out mouse: Roles of CRN7 in vesicle trafficking and F-actin dynamics
Coronins are F-actin binding proteins which belong to an evolutionary conserved family of WD40-repeat proteins. They are widely expressed in cells and tissues and are involved in signal transduction, transcriptional regulation, remodeling of the cytoskeleton and regulation of vesicular trafficking. Here, we focus on mammalian Coronin7 (CRN7), the only `long´ coronin known in mammals, having two WD40-repeat domains which form a highly symmetrical tandem ?-propeller.
CRN7 localizes to the Golgi apparatus where it has a role in protein trafficking and maintenance of Golgi morphology. The role in cytoskeleton remodeling has not been addressed so far. We have generated a CRN7 knockout mouse and established primary fibroblast culture to address the roles of CRN7 in the dynamics of the actin cytoskeleton and to more precisely define its role in vesicular transport. Primary CRN7 KO fibroblasts show a disruption of the Golgi architecture and Golgi-centrosome positioning as well as supernumerary centrosomes. Importantly, we observe an increased cell migration and an accelerated wound closure upon CRN7 deletion and detect a higher F-actin content in CRN7 KO fibroblasts.
Other F-actin related cellular processes like adhesion and spreading seem to be enhanced under CRN7-depleted conditions. The role of CRN7 in anterograde protein export from the ER-Golgi to the plasma membrane is currently being explored.
Taken together, this study will provide an insight into the role of mammalian CRN7 in Golgi trafficking and in cytoskeleton dynamics