Michael C. Wehr

Dr. Michael C. Wehr

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Academic Career Length

22Years (2005-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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27 March 2005 in Nature Neuroscience
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Journal Article
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GSGesine Saher
Gesine Saher
BBBritta Brügger
Britta Brügger
CLCorinna Lappe-Siefke
Corinna Lappe-Siefke
WMWiebke Möbius
Wiebke Möbius
RTRyu-Ichi Tozawa
Ryu-Ichi Tozawa
KNKlaus-Armin Nave
Klaus-Armin Nave
1 February 2010 in Developmental Cell
Verified
Journal Article
Open access
AGAlice Genevet
Alice Genevet
MWMichael C. Wehr
Michael C. Wehr
RBRuth Brain
Ruth Brain
Barry ThompsonBarry Thompson
Barry Thompson
NTNicolas Tapon
Nicolas Tapon
The Salvador (Sav)/Warts (Wts)/Hippo (Hpo) (SWH) network controls tissue growth by inhibiting cell proliferation and promoting apoptosis. The core of the pathway consists of a MST and LATS family kinase cascade that ultimately phosphorylates and inactivates the YAP/Yorkie (Yki) transcription coactivator. The FERM domain proteins Merlin (Mer) and Expanded (Ex) represent one mode of upstream regulation controlling pathway activity. Here, we identify Kibra as a member of the SWH network. Kibra, which colocalizes and associates with Mer and Ex, also promotes the Mer/Ex association. Furthermore, the Kibra/Mer association is conserved in human cells. Finally, Kibra complexes with Wts and kibra depletion in tissue culture cells induces a marked reduction in Yki phosphorylation without affecting the Yki/Wts interaction. We suggest that Kibra is part of an apical scaffold that promotes SWH pathway activity.
29 October 2006 in Nature Methods
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Journal Article
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MWMichael C. Wehr
Michael C. Wehr
RLRico Laage
Rico Laage
UBUlrike Bolz
Ulrike Bolz
TFTobias M Fischer
Tobias M Fischer
SGSylvia Grünewald
Sylvia Grünewald
MRMoritz J. Rossner
Moritz J. Rossner
1 August 2010 in Molecular Cell
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Journal Article
Closed access
PRPaulo S. Ribeiro
Paulo S. Ribeiro
FJFilipe Josué
Filipe Josué
AWAlexander Wepf
Alexander Wepf
MWMichael C. Wehr
Michael C. Wehr
OROliver Rinner
Oliver Rinner
MGMatthias Gstaiger
Matthias Gstaiger
27 January 2009 in PLOS ONE
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Journal Article
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JHJohannes Hirrlinger
Johannes Hirrlinger
Anja SchellerAnja Scheller
Anja Scheller
PHPetra G. Hirrlinger
Petra G. Hirrlinger
BKBeate Kellert
Beate Kellert
WTWannan Tang
Wannan Tang
FKFrank Kirchhoff
Frank Kirchhoff
Cre/LoxP recombination is the gold standard for conditional gene regulation in mice in vivo. However, promoters driving the expression of Cre recombinase are often active in a wide range of cell types and therefore unsuited to target more specific subsets of cells. To overcome this limitation, we designed inactive “split-Cre” fragments that regain Cre activity when overlapping co-expression is controlled by two different promoters. Using transgenic mice and virus-mediated expression of split-Cre, we show that efficient reporter gene activation is achieved in vivo. In the brain of transgenic mice, we genetically defined a subgroup of glial progenitor cells in which the Plp1- and the Gfap-promoter are simultaneously active, giving rise to both astrocytes and NG2-positive glia. Similarly, a subset of interneurons was labelled after viral transfection using Gad67- and Cck1 promoters to express split-Cre. Thus, split-Cre mediated genomic recombination constitutes a powerful spatial and temporal coincidence detector for in vivo targeting.
13 May 2009 in Journal of Neuroscience
Verified
Journal Article
Open access
PDF file
GSGesine Saher
Gesine Saher
SQSusanne Quintes
Susanne Quintes
WMWiebke Möbius
Wiebke Möbius
MWMichael C. Wehr
Michael C. Wehr
EKEva-Maria Krämer-Albers
Eva-Maria Krämer-Albers
KNKlaus Nave
Klaus Nave
Rapid impulse conduction requires electrical insulation of axons by myelin, a cholesterol-rich extension of the glial cell membrane with a characteristic composition of proteins and lipids. Mutations in several myelin protein genes cause endoplasmic reticulum (ER) retention and disease, presumably attributable to failure of misfolded proteins to pass the ER quality control. Because many myelin proteins partition into cholesterol-rich membrane rafts, their interaction with cholesterol could potentially be part of the ER quality control system. Here, we providein vitroandin vivoevidence that the major peripheral myelin protein P0 requires cholesterol for exiting the ER and reaching the myelin compartment. Cholesterol dependency of P0 trafficking in heterologous cells is mediated by a cholesterol recognition/interaction amino acid consensus (CRAC) motif. Mutant mice lacking cholesterol biosynthesis in Schwann cells suffer from severe hypomyelination with numerous uncompacted myelin stretches. This demonstrates that high-level cholesterol coordinates P0 export with myelin membrane synthesis, which is required for the correct stoichiometry of myelin components and for myelin compaction.