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- Publisher Website: 10.1016/j.devcel.2014.10.024
- Scopus: eid_2-s2.0-84919482922
- PMID: 25482883
- WOS: WOS:000346742900010
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Article: Mesenchymal chemotaxis requires selective inactivation of Myosin II at the leading edge via a noncanonical PLCγ/PKCα pathway
Title | Mesenchymal chemotaxis requires selective inactivation of Myosin II at the leading edge via a noncanonical PLCγ/PKCα pathway |
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Authors | |
Issue Date | 2014 |
Citation | Developmental Cell, 2014, v. 31, n. 6, p. 747-760 How to Cite? |
Abstract | Chemotaxis, migration toward soluble chemical cues, is critical for processes such as wound healing and immune surveillance and is exhibited by various cell types, from rapidly migrating leukocytes to slow-moving mesenchymal cells. To study mesenchymal chemotaxis, we observed cell migration in microfluidic chambers that generate stable gradients of platelet-derived growth factor (PDGF). Surprisingly, we found that pathways implicated in amoeboid chemotaxis, such as PI3K and mammalian target ofrapamycin signaling, are dispensable for PDGF chemotaxis. Instead, we find that local inactivation of Myosin IIA, through a noncanonical Ser1/2 phosphorylation of the regulatory light chain, is essential. This site is phosphorylated by PKCα, which is activated by an intracellular gradient of diacylglycerol generated by PLCγ. Using a combination of live imaging and gradients of activators/inhibitors in the microfluidic chambers, we demonstrate that this signaling pathway and subsequent inhibition of Myosin II activity at the leading edge are required for mesenchymal chemotaxis. |
Persistent Identifier | http://hdl.handle.net/10722/311390 |
ISSN | 2023 Impact Factor: 10.7 2023 SCImago Journal Rankings: 5.828 |
PubMed Central ID | |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Asokan, Sreeja B. | - |
dc.contributor.author | Johnson, Heath E. | - |
dc.contributor.author | Rahman, Anisur | - |
dc.contributor.author | King, Samantha J. | - |
dc.contributor.author | Rotty, Jeremy D. | - |
dc.contributor.author | Lebedeva, Irina P. | - |
dc.contributor.author | Haugh, Jason M. | - |
dc.contributor.author | Bear, James E. | - |
dc.date.accessioned | 2022-03-22T11:53:49Z | - |
dc.date.available | 2022-03-22T11:53:49Z | - |
dc.date.issued | 2014 | - |
dc.identifier.citation | Developmental Cell, 2014, v. 31, n. 6, p. 747-760 | - |
dc.identifier.issn | 1534-5807 | - |
dc.identifier.uri | http://hdl.handle.net/10722/311390 | - |
dc.description.abstract | Chemotaxis, migration toward soluble chemical cues, is critical for processes such as wound healing and immune surveillance and is exhibited by various cell types, from rapidly migrating leukocytes to slow-moving mesenchymal cells. To study mesenchymal chemotaxis, we observed cell migration in microfluidic chambers that generate stable gradients of platelet-derived growth factor (PDGF). Surprisingly, we found that pathways implicated in amoeboid chemotaxis, such as PI3K and mammalian target ofrapamycin signaling, are dispensable for PDGF chemotaxis. Instead, we find that local inactivation of Myosin IIA, through a noncanonical Ser1/2 phosphorylation of the regulatory light chain, is essential. This site is phosphorylated by PKCα, which is activated by an intracellular gradient of diacylglycerol generated by PLCγ. Using a combination of live imaging and gradients of activators/inhibitors in the microfluidic chambers, we demonstrate that this signaling pathway and subsequent inhibition of Myosin II activity at the leading edge are required for mesenchymal chemotaxis. | - |
dc.language | eng | - |
dc.relation.ispartof | Developmental Cell | - |
dc.title | Mesenchymal chemotaxis requires selective inactivation of Myosin II at the leading edge via a noncanonical PLCγ/PKCα pathway | - |
dc.type | Article | - |
dc.description.nature | link_to_OA_fulltext | - |
dc.identifier.doi | 10.1016/j.devcel.2014.10.024 | - |
dc.identifier.pmid | 25482883 | - |
dc.identifier.pmcid | PMC4276478 | - |
dc.identifier.scopus | eid_2-s2.0-84919482922 | - |
dc.identifier.volume | 31 | - |
dc.identifier.issue | 6 | - |
dc.identifier.spage | 747 | - |
dc.identifier.epage | 760 | - |
dc.identifier.eissn | 1878-1551 | - |
dc.identifier.isi | WOS:000346742900010 | - |