Four more publications

Aspernig, H., Heimbucher, T., Qi W., Gangurde D., Curic S., Yan Y., Donner von Gromoff E., Baumeister R., Thien A.

Mitochondrial Perturbations Couple mTORC2 to Autophagy in C.elegans

Cell Rep

Kvainickas A., Nägele H., Qi W., Dokládal L., Jimenez-Organz A., Stehl L., Gangurde D., Zhao Q., Hu Z., Dengjel J., De Virgilio C., Baumeister R., Steinberg F.

Retromer and TBC1D5 maintain late endosomal RAB7 domains to enable amino acid-induced mTORC1 signaling

JCell Biol.

Jiang YY., Maier W., Baumeister R., Minevich G., Joachimmiak E., Wloga Dr., Ruan Z., Kannan N., Bocarro S., Bahraini A., VasudeaBahraini A., Vasudevan KK., Lechtreck K., Orias E., Gaertig J.

LF4/MOK and a CDK-related kinase regulate the number and length of cilia in Tetrahymena

PLoS Genet

Weinberg, F., Schulze, E., Fatouros, P., Schmidt, E., Baumeister, R.* and Brummer, T. * (2014)

Expression pattern and first functional characterization of riok-1 in Caenorhabditis elegans,
Gene Exp Pattern * corresponding authors

Wolf, T., Q, W., Schindler, V., Runkel, E.D., and Baumeister, R. (2014)
Doxycyclin ameliorates a starvation-induced germline tumor in C. elegans daf-18/PTEN mutants.
Exp Gerontol. 2014 Apr 15. pii: S0531-5565(14)00123-5.
doi: 10.1016/j.exger.2014.04.002.

Runkel, ED., Baumeister, R., and Schulze, E (2014)
Mitochondrial stress: Balancing friend and foe.
Exp Gerontol. 2014 Mar 3. pii: S0531-5565(14)00070-9.
doi: 10.1016/j.exger.2014.02.013. Review

Cabello, J., Sämann, J., Gómez-Orte, E., Erazo, T., Coppa, A., Pujol, A., Büssing, I, Schulze, B, Lizcano, J.M., Ferrer*, I., Baumeister*, R., Dalfo, E. (2014)
pdr-1/hParkin negatively regulates the phagocytosis of apoptotic cell corpses in C. elegans.
Cell Death Dis. Mar 13;5:e1120. doi: 10.1038/cddis.2014.57. * cocorresponding authors

Cell publication “Inhibition of mTORC1 by Astrin and Stress Granules Prevents Apoptosis in Cancer Cells.”

Mammalian target of rapamycin complex 1 (mTORC1) controls growth and survival in response to metabolic cues. Oxidative stress affects mTORC1 via inhibitory and stimulatory inputs. Whereas downregulation of TSC1-TSC2 activates mTORC1 upon oxidative stress, the molecular mechanism of mTORC1 inhibition remains unknown. We identified astrin as an essential negative mTORC1 regulator in the cellular stress response. Upon stress, astrin inhibits mTORC1 association and recruits the mTORC1 component raptor to stress granules (SGs), thereby preventing mTORC1-hyper-activation-induced apoptosis. In turn, balanced mTORC1 activity enables expression of stress factors. By identifying astrin as a direct molecular link between mTORC1, SG assembly, and the stress response, we establish a unifying model of mTORC1 inhibition and activation upon stress. Importantly, we show that in cancer cells, apoptosis suppression during stress depends on astrin. Being frequently upregulated in tumors, astrin is a potential clinically relevant target to sensitize tumors to apoptosis.

Inhibition of mTORC1 by Astrin and Stress Granules Prevents Apoptosis in Cancer Cells. Kathrin Thedieck, Birgit Holzwarth, Mirja Tamara Prentzell, Christopher Boehlke, Kathrin Kläsener, Stefanie Ruf, Annika Sonntag, Lars Maerz, Sushma-Nagaraja Grellscheid, Elisabeth Kremmer, Roland Nitschke, E. Wolfgang Kuehn, Johan W. Jonker, Albert K. Groen, Michael Reth, Michael N. Hall, Ralf Baumeister Cell – 15 August 2013 (Vol. 154, Issue 4, pp. 859-874)

For more info see this press release issued by the University of Freiburg.

SnAvi – a new tandem tag for high-affinity protein-complex purification

The SnAvi-tag is a novel in-vivo fluorescent tag combining several features to allow for tandem-purification, western blotting and in-vivo subcellular localization of proteins fused to it. It has been shown to work in expression systems as diverse as C. elegansE. Coli and vertebrate cells. For further information see Schäffer et al., Nucleic Acids Res. 2010 Jan 4: SnAvi–a new tandem tag for high-affinity protein-complex purification (PMID: 20047968)