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Rho1 regulates adherens junction remodeling by promoting recycling endosome formation through activation of myosin II.

Yashiro H, Loza AJ, Skeath JB, Longmore GD - Mol. Biol. Cell (2014)

Bottom Line: We demonstrate that Rho1 also influences AJ remodeling by regulating the formation of DE-cadherin-containing, Rab11-positive recycling endosomes in Drosophila postmitotic pupal eye epithelia.This effect of Rho1 is mediated through Rok-dependent, but not MLCK-dependent, stimulation of myosin II activity yet independent of its effects upon actin remodeling.This work identifies spatially distinct functions for Rho1 in the regulation of DE-cadherin-containing vesicular trafficking during AJ remodeling in live epithelia.

View Article: PubMed Central - PubMed

Affiliation: ICCE Institute, Washington University School of Medicine, St. Louis, MO 63110 Department of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, MO 63110 Department of Developmental Biology, Washington University School of Medicine, St. Louis, MO 63110.

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Proposed working model of Rho1-dependent regulation of REs. Rho1 functions on the surface of CREs to regulate RE formation by activating MLC and myosin II contractility. The activity of myosin II during this process is stimulated by the immediate downstream effector of Rho1, Rok, and phosphatase MBS but not MLCK. The effect of Rok on actin turnover through regulation of LIMK and cofilin inhibition is not required for RE formation.
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Figure 7: Proposed working model of Rho1-dependent regulation of REs. Rho1 functions on the surface of CREs to regulate RE formation by activating MLC and myosin II contractility. The activity of myosin II during this process is stimulated by the immediate downstream effector of Rho1, Rok, and phosphatase MBS but not MLCK. The effect of Rok on actin turnover through regulation of LIMK and cofilin inhibition is not required for RE formation.

Mentions: This work demonstrates that Rho1 regulates AJ remodeling in live Drosophila pupal eye epithelia through spatially distinct control of DE-cadherin trafficking within PECs. Previous work has shown that Rho1 controls DE-cadherin endocytosis by limiting Cdc42 activity, presumably at or near the plasma membrane (Warner and Longmore, 2009b). Now we show that Rho1 also regulates a later stage of DE-cadherin trafficking from Rab5- and Rab11-positive vesicles to Rab11-positive REs. Unlike Rho1’s effect upon DE-cadherin endocytosis, Rho1-mediated RE production occurs through Rok-dependent activation of myosin II, possibly on intracellular vesicles (Figure 7) and independent of the Cdc42/Par6/aPKC complex. Similar to Rho1’s regulation of endocytosis, Rho1-Rok-myosin II regulation of RE production did not appear to depend uniquely on Rho1’s effects upon actin turnover.


Rho1 regulates adherens junction remodeling by promoting recycling endosome formation through activation of myosin II.

Yashiro H, Loza AJ, Skeath JB, Longmore GD - Mol. Biol. Cell (2014)

Proposed working model of Rho1-dependent regulation of REs. Rho1 functions on the surface of CREs to regulate RE formation by activating MLC and myosin II contractility. The activity of myosin II during this process is stimulated by the immediate downstream effector of Rho1, Rok, and phosphatase MBS but not MLCK. The effect of Rok on actin turnover through regulation of LIMK and cofilin inhibition is not required for RE formation.
© Copyright Policy - creative-commons
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4230585&req=5

Figure 7: Proposed working model of Rho1-dependent regulation of REs. Rho1 functions on the surface of CREs to regulate RE formation by activating MLC and myosin II contractility. The activity of myosin II during this process is stimulated by the immediate downstream effector of Rho1, Rok, and phosphatase MBS but not MLCK. The effect of Rok on actin turnover through regulation of LIMK and cofilin inhibition is not required for RE formation.
Mentions: This work demonstrates that Rho1 regulates AJ remodeling in live Drosophila pupal eye epithelia through spatially distinct control of DE-cadherin trafficking within PECs. Previous work has shown that Rho1 controls DE-cadherin endocytosis by limiting Cdc42 activity, presumably at or near the plasma membrane (Warner and Longmore, 2009b). Now we show that Rho1 also regulates a later stage of DE-cadherin trafficking from Rab5- and Rab11-positive vesicles to Rab11-positive REs. Unlike Rho1’s effect upon DE-cadherin endocytosis, Rho1-mediated RE production occurs through Rok-dependent activation of myosin II, possibly on intracellular vesicles (Figure 7) and independent of the Cdc42/Par6/aPKC complex. Similar to Rho1’s regulation of endocytosis, Rho1-Rok-myosin II regulation of RE production did not appear to depend uniquely on Rho1’s effects upon actin turnover.

Bottom Line: We demonstrate that Rho1 also influences AJ remodeling by regulating the formation of DE-cadherin-containing, Rab11-positive recycling endosomes in Drosophila postmitotic pupal eye epithelia.This effect of Rho1 is mediated through Rok-dependent, but not MLCK-dependent, stimulation of myosin II activity yet independent of its effects upon actin remodeling.This work identifies spatially distinct functions for Rho1 in the regulation of DE-cadherin-containing vesicular trafficking during AJ remodeling in live epithelia.

View Article: PubMed Central - PubMed

Affiliation: ICCE Institute, Washington University School of Medicine, St. Louis, MO 63110 Department of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, MO 63110 Department of Developmental Biology, Washington University School of Medicine, St. Louis, MO 63110.

Show MeSH
Related in: MedlinePlus