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Costars, a Dictyostelium protein similar to the C-terminal domain of STARS, regulates the actin cytoskeleton and motility. | LitMetric

AI Article Synopsis

  • A new gene called costars (cosA) was identified in a chemotaxis mutant of Dictyostelium discoideum, which is crucial for regulating cell migration.
  • The Costars protein is highly conserved across various species and resembles the C-terminal region of a mammalian protein, STARS, that influences actin binding and Rho GTPase activation.
  • Cells lacking cosA showed impaired motility, abnormal actin distribution, and excessive pseudopod formation, while reintroducing cosA restored normal function and highlighted its role in actin dynamics and cell movement.

Article Abstract

Through analysis of a chemotaxis mutant obtained from a genetic screen in Dictyostelium discoideum, we have identified a new gene involved in regulating cell migration and have named it costars (cosA). The 82 amino acid Costars protein sequence appears highly conserved among diverse species, and significantly resembles the C-terminal region of the striated muscle activator of Rho signaling (STARS), a mammalian protein that regulates the serum response factor transcriptional activity through actin binding and Rho GTPase activation. The cosA-null (cosA(-)) cells formed smooth plaques on bacterial lawns, produced abnormally small fruiting bodies when developed on the non-nutrient agar and displayed reduced migration towards the cAMP source in chemotactic assays. Analysis of cell motion in cAMP gradients revealed decreased speed but wild-type-like directional persistence of cosA(-) cells, suggesting a defect in the cellular machinery for motility rather than for chemotactic orientation. Consistent with this notion, cosA(-) cells exhibited changes in the actin cytoskeleton, showing aberrant distribution of F-actin in fluorescence cell staining and an increased amount of cytoskeleton-associated actin. Excessive pseudopod formation was also noted in cosA(-) cells facing chemoattractant gradients. Expressing cosA or its human counterpart mCostars eliminated abnormalities of cosA(-) cells. Together, our results highlight a role for Costars in modulating actin dynamics and cell motility.

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Source
http://dx.doi.org/10.1242/jcs.064709DOI Listing

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