Specialization of actin isoforms derived from the loss of key interactions with regulatory factors Article Swipe
Micaela Boiero Sanders
,
Christopher P. Toret
,
Adrien Antkowiak
,
Robert Robinson
,
Alphée Michelot
·
YOU?
·
· 2021
· Open Access
·
· DOI: https://doi.org/10.1101/2021.02.09.430555
YOU?
·
· 2021
· Open Access
·
· DOI: https://doi.org/10.1101/2021.02.09.430555
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.
Related Topics
Concepts
Cell biology
Actin
Actin cytoskeleton
Formins
Actin remodeling
Biology
Heterologous
Cytoskeleton
Gene isoform
Actin remodeling of neurons
Heterologous expression
MDia1
Actin-binding protein
Cell
Genetics
Gene
Recombinant DNA
Metadata
- Type
- preprint
- Language
- en
- Landing Page
- https://doi.org/10.1101/2021.02.09.430555
- https://www.biorxiv.org/content/biorxiv/early/2021/02/11/2021.02.09.430555.full.pdf
- OA Status
- green
- References
- 70
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W3127076683
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W3127076683Canonical identifier for this work in OpenAlex
- DOI
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https://doi.org/10.1101/2021.02.09.430555Digital Object Identifier
- Title
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Specialization of actin isoforms derived from the loss of key interactions with regulatory factorsWork title
- Type
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preprintOpenAlex work type
- Language
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enPrimary language
- Publication year
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2021Year of publication
- Publication date
-
2021-02-11Full publication date if available
- Authors
-
Micaela Boiero Sanders, Christopher P. Toret, Adrien Antkowiak, Robert Robinson, Alphée MichelotList of authors in order
- Landing page
-
https://doi.org/10.1101/2021.02.09.430555Publisher landing page
- PDF URL
-
https://www.biorxiv.org/content/biorxiv/early/2021/02/11/2021.02.09.430555.full.pdfDirect link to full text PDF
- Open access
-
YesWhether a free full text is available
- OA status
-
greenOpen access status per OpenAlex
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https://www.biorxiv.org/content/biorxiv/early/2021/02/11/2021.02.09.430555.full.pdfDirect OA link when available
- Concepts
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Cell biology, Actin, Actin cytoskeleton, Formins, Actin remodeling, Biology, Heterologous, Cytoskeleton, Gene isoform, Actin remodeling of neurons, Heterologous expression, MDia1, Actin-binding protein, Cell, Genetics, Gene, Recombinant DNATop concepts (fields/topics) attached by OpenAlex
- Cited by
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0Total citation count in OpenAlex
- References (count)
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70Number of works referenced by this work
- Related works (count)
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10Other works algorithmically related by OpenAlex
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