Uni-Tübingen

P7: Identification of cGMP-dependent protein kinase I substrates mediating sensory axon bifurcation

Aims

Further dissection of the CNP-induced cGMP signaling cascade that regulates sensory axon bifurcation for a better mechanistic understanding of axonal growth, guidance and branching.

cGMP and Axon Branching

Questions and Methods

Boston Internship

Blanton Lab

In the Blanton lab in Boston, the doctoral researchers will receive training in several biochemical screening methods for cGKI substrates, including GST-pulldown studies using a cGKI-LZM mutant protein, direct cGMP pulldowns, and standard immunoprecipitations.

These techniques will also be instrumental for the validation of putative novel interaction partners of cGKI resulting from analyses using the analog-sensitive kinase mutant and the SILAC approach (see above).

Boston Co-mentor

Assist. Prof. Robert M. Blanton, MD

Link to boston researcher lab

Doctoral Student

Alexandra Böttcher

Alexandra Böttcher started her studies in the field of biochemistry at Ulm University, conducting her Bachelor's thesis on electrophysiological analysis of the dopamine response of substantia nigra neurons. Taking the opportunity to follow her interest in neurophysiological research, she continued at Ulm University and earned her Master's degree in Molecular and Translational Neuroscience. Her thesis focused on the influence of the gut microbiome on chronic psychosocial stress. Aiming to utilize innovative biochemical methodology in neuroscientific research, Alexandra joined the group of Hannes Schmidt as a doctoral student. Her main research interest lies in the role of cGMP signaling in sensory axon branching during embryonal spinal cord development.


Key Publications

Schmidt H, Stonkute A, Jüttner R, Koesling D, Friebe A, Rathjen FG. C-type natriuretic peptide (CNP) is a bifurcation factor for sensory neurons. Proc Natl Acad Sci U S A. 2009;106:16847-52

Ter-Avetisyan G, Rathjen FG, Schmidt H.  Bifurcation of axons from cranial sensory neurons is disabled in the absence of Npr2-induced cGMP signaling. J Neurosci. 2014;34:737-47