Specialization of actin isoforms derived from the loss of key interactions with regulatory factors

Micaela Boiero Sanders, Christopher P. Toret, Audrey Guillotin, Adrien Antkowiak, Thomas Vannier, Robert C. Robinson, Alphée Michelot

Research output: Contribution to journalArticlepeer-review

Abstract

A paradox of eukaryotic cells is that while some species assemble a complex actin cytoskeleton from a single ortholog, other species utilize a greater diversity of actin isoforms. The physiological consequences of using different actin isoforms, and the molecular mechanisms by which highly conserved actin isoforms are segregated into distinct networks, are poorly known. Here, we sought to understand how a simple biological system, composed of a unique actin and a limited set of actin-binding proteins, reacts to a switch to heterologous actin expression. Using yeast as a model system and biomimetic assays, we show that such perturbation causes drastic reorganization of the actin cytoskeleton. Our results indicate that defective interaction of a heterologous actin for important regulators of actin assembly limits certain actin assembly pathways while reinforcing others. Expression of two heterologous actin variants, each specialized in assembling a different network, rescues cytoskeletal organization and confers resistance to external perturbation. Hence, while species using a unique actin have homeostatic actin networks, actin assembly pathways in species using several actin isoforms may act more independently.

Original languageEnglish
Article numbere107982
JournalEMBO Journal
Volume41
Issue number5
DOIs
Publication statusPublished - Mar 1 2022

Keywords

  • actin cytoskeleton
  • actin isoforms
  • actin-binding proteins
  • biomimetism
  • Saccharomyces cerevisiae

ASJC Scopus subject areas

  • Neuroscience(all)
  • Molecular Biology
  • Biochemistry, Genetics and Molecular Biology(all)
  • Immunology and Microbiology(all)

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