What is it about?

Our experiments have determined why blocking of microtubule acetylation causes mitotic abnormalities. There is much current interest in post-translational modifications of tubulin and of the microtubules formed from tubulin. Much has been found out using molecular genetic and other tools, but little is known about what the modified microtubules do. This generalization applies to post-translationally modified spindle microtubules: we barely know which post-translationally-modified tubulins are present in spindles let alone what they do. In this article we have studied acetylated spindle microtubules using a unique system. In the crane-fly spermatocytes that we studied, the only acetylated microtubules in the cells are those in the kinetochore microtubules, the microtubules that connect the kinetochores to their poles. We know that the kinetochore microtubules must be depolymerized in order for chromosomes to move to the poles. And we know that acetylation of microtubules stabilizes them against most agents (e.g., cold, or microtubule depolymerising agents). But no theory of chromosome movement takes into account modified tubulin. We reckoned that unless acetylated microtubules were deacetylated during anaphase, the acetylation of kinetochore microtubules would block their depolymerization.

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Why is it important?

By understanding the role of acetylation/deacetylation of kinetochore microtubules in mitosis regulation, we can get some insights into inform the development of new treatments that may be less toxic relative to traditional ones. Investigating the reason of chromosome mis segregation may help us to prevent the progress of several diseases such as neurodegenerative diseases.

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This page is a summary of: Blocking microtubule deacetylation inhibits anaphase chromosome movements in crane-fly spermatocytes, PLOS One, December 2024, PLOS,
DOI: 10.1371/journal.pone.0311691.
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