# Dynein dynamics at the microtubule plus-ends and cortex during division   in the C. $\textit{elegans}$ zygote

**Authors:** Ruddi Rodriguez Garcia, Laurent Chesneau, Sylvain Pastezeur, Julien, Roul, Marc Tramier, Jacques P\'ecr\'eaux

arXiv: 1703.07610 · 2017-11-07

## TL;DR

This study investigates dynein dynamics during asymmetric cell division in C. elegans, revealing its microtubule plus-end accumulation, cortical behavior, and role in force generation and polarity regulation.

## Contribution

It uncovers the mechanism of dynein targeting to microtubule plus-ends via EBP-2 and dynactin, and characterizes its cortical motion and force-generating behavior during division.

## Key findings

- Dynein accumulates at microtubule plus-ends via EBP-2 and dynactin.
- Dynein exhibits directed and diffusive-like cortical tracks, with diffusive tracks indicating force generation.
- Posterior enrichment of force-generating dynein correlates with polarity-related force imbalance.

## Abstract

During asymmetric cell division, dynein generates forces, which position the spindle to reflect polarity and ensure correct daughter cell fates. The transient cortical localization of dynein raises the question of its targeting. We found that it accumulates at the microtubule plus-ends like in budding yeast, indirectly hitch-hiking on $\text{EBP-2}^{\text{EB1}}$ likely via dynactin. Importantly, this mechanism, which modestly accounts for cortical forces, does not transport dynein, which displays the same binding/unbinding dynamics as $\text{EBP-2}^{\text{EB1}}$. At the cortex, dynein tracks can be classified as having either directed or diffusive-like motion. Diffusive-like tracks reveal force-generating dyneins. Their densities are higher on the posterior tip of the embryos, where $\text{GPR-1/2}^{\text{LGN}}$ concentrate, but their durations are symmetric. Since dynein flows to the cortex are non-polarized, we suggest that this posterior enrichment increases dynein binding, thus accounts for the force imbalance reflecting polarity, and supplements the regulation of mitotic progression via the non-polarized detachment rate.

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Source: https://tomesphere.com/paper/1703.07610