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Loss of Dictyostelium HSPC300 causes a scar-like phenotype and loss of SCAR protein.

ABSTRACT: SCAR/WAVE proteins couple signalling to actin polymerization, and are thus fundamental to the formation of pseudopods and lamellipods. They are controlled as part of a five-membered complex that includes the tiny HSPC300 protein. It is not known why SCAR/WAVE is found in such a large assembly, but in Dictyostelium the four larger subunits have different, clearly delineated functions.We have generated Dictyostelium mutants in which the HSPC300 gene is disrupted. As has been seen in other regulatory complex mutants, SCAR is lost in these cells, apparently by a post-translational mechanism, though PIR121 levels do not change. HSPC300 knockouts resemble scar mutants in slow migration, roundness, and lack of large pseudopods. However hspc300-colonies on bacteria are larger and more similar to wild type, suggesting that some SCAR function can survive without HSPC300. We find no evidence for functions of HSPC300 outside the SCAR complex.HSPC300 is essential for most SCAR complex functions. The phenotype of HSPC300 knockouts is most similar to mutants in scar, not the other members of the SCAR complex, suggesting that HSPC300 acts most directly on SCAR itself.

SUBMITTER: Pollitt AY

PROVIDER: S-EPMC2652429 | biostudies-literature | 2009 Feb

REPOSITORIES: biostudies-literature

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Loss of Dictyostelium HSPC300 causes a scar-like phenotype and loss of SCAR protein.

Pollitt Alice Y AY Insall Robert H RH

BMC cell biology 20090219

<h4>Background</h4>SCAR/WAVE proteins couple signalling to actin polymerization, and are thus fundamental to the formation of pseudopods and lamellipods. They are controlled as part of a five-membered complex that includes the tiny HSPC300 protein. It is not known why SCAR/WAVE is found in such a large assembly, but in Dictyostelium the four larger subunits have different, clearly delineated functions.<h4>Results</h4>We have generated Dictyostelium mutants in which the HSPC300 gene is disrupted. ...[more]

PMID: 19228419

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Project description:Cyclic AMP (cAMP) is an important intracellular signaling molecule for many G protein-mediated signaling pathways but the specificity of cAMP signaling in cells with multiple signaling pathways is not well-understood. In Dictyostelium, at least two different G protein signaling pathways, mediated by the G?2 and G?4 subunits, are involved with cAMP accumulation, spore production, and chemotaxis and the stimulation of these pathways results in the activation of ERK2, a mitogen-activated protein kinase that can down regulate the cAMP-specific phosphodiesterase RegA. The regA gene was disrupted in g?2(?) and g?4(?) cells to determine if the absence of this phosphodiesterase rescues the development of these G protein mutants as it does for erk2(?) mutants. There gA(?) mutation had no major effects on developmental morphology but enriched the distribution of the G? mutant cells to the prespore/prestalk border in chimeric aggregates. The loss of RegA function had no effect on G?4- mediated folate chemotaxis. However, the regA gene disruption in g?4(?) cells, but not in g?2(?) cells, resulted in a substantial rescue and acceleration of spore production. This rescue in sporulation required cell autonomous signaling because the precocious sporulation could not be induced through intercellular signaling in chimeric aggregates. However, intercellular signals from regA(?) strains increased the expression of the prestalk gene ecmB and accelerated the vacuolization of stalk cells. Intercellular signaling from the g?4(?)regA(?) strain did not induce ecmA gene expression indicating cell-type specificity in the promotion of prestalk cell development. regA gene disruption in a G?4(HC) (G?4 overexpression) strain did not result in precocious sporulation or stalk cell development indicating that elevated G?4 subunit expression can mask regA(?) associated phenotypes even when provided with wild-type intercellular signaling. These findings indicate that the G?2 and G?4-mediated pathways provide different contributions to the development of spores and stalk cells and that the absence of RegA function can bypass some but not all defects in G protein regulated spore development.

Dataset Information

Loss of Dictyostelium HSPC300 causes a scar-like phenotype and loss of SCAR protein.

Publications

Loss of Dictyostelium HSPC300 causes a scar-like phenotype and loss of SCAR protein.

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