Please inhibit responsibly: Natural and synthetic actin toxins as useful tools in cell biology.

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2025-10

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Abstract

The actin cytoskeleton drives many critical cell functions, including motility, division, and vesicular trafficking. To fulfill these functions, actin networks are dynamic and tightly regulated by dozens of proteins that cause actin to assemble and disassemble at the proper time and place. Given the importance of actin to a cell's biology, it is not surprising that some organisms produce toxins that target actin dynamics to incapacitate prey, win turf wars, or as a defense against predation. For decades, cell biologists have leveraged these toxins and synthesized new ones to cause defects in the structure and function of the actin cytoskeleton. Here, we provide an overview of commonly used actin inhibitors and their origins, as well as best practices for their use in biological studies.

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Animals, Humans, Actins, Toxins, Biological, Cell Biology, Actin Cytoskeleton

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Published Version (Please cite this version)

10.1091/mbc.e25-05-0264

Publication Info

Velle, Katrina B, and Masayuki Onishi (2025). Please inhibit responsibly: Natural and synthetic actin toxins as useful tools in cell biology. Molecular biology of the cell, 36(10). p. pe7. 10.1091/mbc.e25-05-0264 Retrieved from https://hdl.handle.net/10161/33628.

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Scholars@Duke

Onishi

Masayuki Onishi

Assistant Professor of Biology

The overall goal of the Onishi lab is to understand the fundamental core mechanisms of eukaryotic cell division that have been conserved throughout the evolution from the last eukaryotic common ancestor.  To this end, the lab currently uses the unicellular model green alga Chlamydomonas reinhardtii, which is evolutionarily close to plants yet divide like animals by forming a cleavage furrow.  Strikingly, unlike animals, this organism does not have a non-muscle type-II myosin that has been believed to be essential for furrowing.  In fact, animals, fungi, slime molds, and related species are the exceptions in that they have this myosin motor protein, and the vast majority of the eukaryotes divide by some mechanism that we don't fully understand.  Our work aims to understand how the cells without type-II myosin manage to form a cleavage furrow, which should shed light on the questions such as:
(1) How did the ancestral cells divide?
(2) What was the evolutionary advantage of type-II myosin when it emerged in the select lineage?
(3) How did the unique evolution into modern land plants happen?


In the lab, we use the power of genetics, genomics, and molecular and cellular biology.  Specific questions include, but not limited to:
How do the three cytoskeletal systems (actin, microtubules, and septin) contribute to cell division?
What is the involvement of extracellular matrix and the ESCRT system?
How do the known and yet-to-be known genes interact with one another to control cell division?



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