RhoA is dispensable for skin development, but crucial for contraction and directed migration of keratinocytes

Jackson, Ben; Peyrollier, Karine; Pedersen, Esben; Basse, Astrid L.; Karlsson, Richard; Wang, Zhipeng; Lefever, Tine; Ochsenbein, Alexandra M.; Schmidt, Gudula; Aktories, Klaus; Stanley, Alanna; Quondamatteo, Fabio; Ladwein, Markus; Rottner, Klemens; Hengel, Jolanda van; Brakebusch, Cord

doi:10.1091/mbc.e09-10-0859

Cited by 132 publications

(157 citation statements)

References 45 publications

Supporting

Mentioning

141

Contrasting

Order By: Relevance

“…Mice-Myeloid-restricted RhoA (ras homolog gene family, member A; Mouse Genome Informatics (MGI): 1096342) knock-out mice were generated by crossing floxed RhoA (34) and LysM-Cre (35) mice. These mice were further crossed with RhoB (ras homolog gene family, member A; MGI: 107949) knock-out mice (28) to generate RhoA (myeloid-restricted)/ RhoB double knock-out mice.…”

Section: Methodsmentioning

confidence: 99%

“…1, E and F). Up-regulation of RhoB levels has been observed in RhoA-deficient keratinocytes (34) and may be an indicator that RhoB functionally compensates for RhoA deficiency.…”

Section: Rhoa and Rhob But Not Rhoc Are Expressed In Mousementioning

confidence: 99%

“…In contrast to RhoB and RhoC, global deletion of RhoA in mice is lethal (32). Deletion of RhoA in mouse embryonic fibroblasts impaired mitosis (33), whereas deletion of RhoA in keratinocytes impaired directed migration, which could not be explained by disruption of ROCK signaling (34).…”

mentioning

confidence: 98%

See 2 more Smart Citations

Mouse Macrophages Completely Lacking Rho Subfamily GTPases (RhoA, RhoB, and RhoC) Have Severe Lamellipodial Retraction Defects, but Robust Chemotactic Navigation and Altered Motility

Königs

Jennings

Vogl

et al. 2014

Journal of Biological Chemistry

Self Cite

View full text Add to dashboard Cite

Background:RhoA is strongly implicated in cell motility. Results: Macrophages lacking RhoA or RhoB have mild phenotypes, whereas double mutants, which also lack RhoC, exhibit severe cytoskeletal defects, but robust chemotaxis. Conclusion: RhoA and RhoB have overlapping functions in tail and lamellipodial membrane retraction, but are not critical for motility. Significance: The Rho subfamily is largely redundant for "front end" functions of motility and chemotaxis.

show abstract

Section: Methodsmentioning

confidence: 99%

“…1, E and F). Up-regulation of RhoB levels has been observed in RhoA-deficient keratinocytes (34) and may be an indicator that RhoB functionally compensates for RhoA deficiency.…”

Section: Rhoa and Rhob But Not Rhoc Are Expressed In Mousementioning

confidence: 99%

See 1 more Smart Citation

Mouse Macrophages Completely Lacking Rho Subfamily GTPases (RhoA, RhoB, and RhoC) Have Severe Lamellipodial Retraction Defects, but Robust Chemotactic Navigation and Altered Motility

Königs

Jennings

Vogl

et al. 2014

Journal of Biological Chemistry

Self Cite

View full text Add to dashboard Cite

show abstract

“…However, in knockout studies, RhoBnull and RhoC-null mice are viable and have normal development (17,18). Recently, conditional deletion of RhoA in the developing skin was reported, but the mutant mice did not show any obvious phenotypes in vivo (19). Therefore, RhoA and its close isoforms, RhoB and RhoC, may have redundant functions in skin development.…”

Section: Cns Development | Cell Adhesionmentioning

confidence: 99%

Loss of RhoA in neural progenitor cells causes the disruption of adherens junctions and hyperproliferation

Katayama

Meléndez

Baumann

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

100

138

View full text Add to dashboard Cite

The organization of neural progenitors in the developing mammalian neuroepithelium is marked by cadherin-based adherens junctions. Whereas RhoA, a founding member of the small Rho GTPase family, has been shown to play important roles in epithelial adherens junctions, its physiological roles in neural development remain uncertain due to the lack of specific loss-of-function studies. Here, we show that RhoA protein accumulates at adherens junctions in the developing mouse brain and colocalizes to the cadherin–catenin complex. Conditional deletion of RhoA in midbrain and forebrain neural progenitors using Wnt1-Cre and Foxg1-Cre mice, respectively, disrupts apical adherens junctions and causes massive dysplasia of the brain. Furthermore, RhoA -deficient neural progenitor cells exhibit accelerated proliferation, reduction of cell- cycle exit, and increased expression of downstream target genes of the hedgehog pathway. Consequently, both lines of conditional RhoA -deficient embryos exhibit expansion of neural progenitor cells and exencephaly-like protrusions. These results demonstrate a critical role of RhoA in the maintenance of apical adherens junctions and the regulation of neural progenitor proliferation in the developing mammalian brain.

show abstract

“…Different from that in MEF cells (12), keratin-5 Cre-driven rhoA deletion in keratinocytes in vivo was sufficient to reduce phosphorylation of MLC and cofilin (19). Primary keratinocyte culture showed additional defects upon rhoA deletion: impaired junction maturation, a mild cytokinesis defect, and decreased directional migration.…”

Section: Signaling Role Of Rhoa Revealed By Gene Targeting In Micementioning

confidence: 76%

Cell Type-specific Signaling Function of RhoA GTPase: Lessons from Mouse Gene Targeting

Zhou

Zheng

2013

Journal of Biological Chemistry

View full text Add to dashboard Cite

RhoA is dispensable for skin development, but crucial for contraction and directed migration of keratinocytes

Cited by 132 publications

References 45 publications

Mouse Macrophages Completely Lacking Rho Subfamily GTPases (RhoA, RhoB, and RhoC) Have Severe Lamellipodial Retraction Defects, but Robust Chemotactic Navigation and Altered Motility

Mouse Macrophages Completely Lacking Rho Subfamily GTPases (RhoA, RhoB, and RhoC) Have Severe Lamellipodial Retraction Defects, but Robust Chemotactic Navigation and Altered Motility

Loss of RhoA in neural progenitor cells causes the disruption of adherens junctions and hyperproliferation

Cell Type-specific Signaling Function of RhoA GTPase: Lessons from Mouse Gene Targeting

Contact Info

Product

Resources

About