How to tune spindle size relative to cell size?

Rieckhoff, Elisa Maria; Ishihara, Keisuke; Brugués, Jan

doi:10.1016/j.ceb.2019.06.007

Cited by 7 publications

(5 citation statements)

References 41 publications

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“…Kinases such as Cdk1, MARK, and Nek may regulate the affinity of these MAPs (Adib et al 2018;Ookata et al 1997;Chang et al 2001;Drewes et al 1992;Illenberger et al 1996;Drewes et al 1997). Our current model is a useful starting point for future studies that consider complex multispecies dynamics of cytoskeletal self-organization including the mitotic spindle (Hazel et al 2013;Good et al 2013;Rieckhoff, Ishihara, and Brugués 2019;Rieckhoff et al 2020). Second, while most MAPs that slow down depolymerization have been reported to accelerate polymerization in minimal conditions (Drechsel et al 1992;Andersen et al 1994;Andersen and Karsenti 1997), we observed little regulation of polymerization rate in our aster reactions.…”

Section: Limiting Component Hypothesis For the Spatial Regulation Of mentioning

confidence: 99%

Spatial variation of microtubule depolymerization in large asters

Ishihara

Decker

Caldas

et al. 2021

MBoC

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Microtubule plus end depolymerization rate is a potentially important target of physiological regulation, but it has been challenging to measure, so its role in spatial organization is poorly understood. Here we apply a method for tracking plus ends based on time difference imaging to measure depolymerization rates in large interphase asters growing in Xenopus egg extract. We observed strong spatial regulation of depolymerization rates, which were higher in the aster interior compared to the periphery, and much less regulation of polymerization or catastrophe rates. We interpret these data in terms of a limiting component model, where aster growth results in lower levels of soluble tubulin and MAPs in the interior cytosol compared to that at the periphery. The steady-state polymer fraction of tubulin was ∼30%, so tubulin is not strongly depleted in the aster interior. We propose that the limiting component for microtubule assembly is a MAP that inhibits depolymerization, and that egg asters are tuned to low microtubule density. [Media: see text] [Media: see text] [Media: see text] [Media: see text] [Media: see text]

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Section: Limiting Component Hypothesis For the Spatial Regulation Of mentioning

confidence: 99%

Spatial variation of microtubule depolymerization in large asters

Ishihara

Decker

Caldas

et al. 2021

MBoC

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“…MTs undergo phases of growth and shrinkage known as dynamic instability (T. Mitchison & Kirschner, 1984). A variety of MT binding and regulatory proteins affects MT dynamics and consequently spindle length (Rieckhoff, Ishihara, & Brugues, 2019). Spindles are responsible for equal segregation of chromosomes between daughter cells during cell division.…”

Section: Mitotic Spindlesmentioning

confidence: 99%

Organelle size scaling over embryonic development

Wesley

Mishra

Levy

2020

WIREs Developmental Biology

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“…This decreasing density would inherently reduce the probability of kinetochore capture, and therefore increase mitotic spindle assembly duration as spindles get longer [ 79 ]. Thus, in large cells that assemble spindles longer than 30 µm, the number of spindle microtubules must be adjusted along the spindle length in order to maintain microtubule density [ 8 , 39 , 92 , 93 ]. The increase in spindle microtubule number within the spindle could also participate in a potential temporal scaling mechanism by shortening the duration of chromosome capture [ 79 ] and therefore ensuring that spindle assembly duration is uncoupled from spindle size and cell dimensions.…”

Section: Mechanisms Ensuring Spatial and Temporal Scaling Of The Mitotic Spindlementioning

confidence: 99%

Spatial and Temporal Scaling of Microtubules and Mitotic Spindles

Lacroix

Dumont

2022

Cells

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During cell division, the mitotic spindle, a macromolecular structure primarily comprised of microtubules, drives chromosome alignment and partitioning between daughter cells. Mitotic spindles can sense cellular dimensions in order to adapt their length and mass to cell size. This scaling capacity is particularly remarkable during early embryo cleavage when cells divide rapidly in the absence of cell growth, thus leading to a reduction of cell volume at each division. Although mitotic spindle size scaling can occur over an order of magnitude in early embryos, in many species the duration of mitosis is relatively short, constant throughout early development and independent of cell size. Therefore, a key challenge for cells during embryo cleavage is not only to assemble a spindle of proper size, but also to do it in an appropriate time window which is compatible with embryo development. How spatial and temporal scaling of the mitotic spindle is achieved and coordinated with the duration of mitosis remains elusive. In this review, we will focus on the mechanisms that support mitotic spindle spatial and temporal scaling over a wide range of cell sizes and cellular contexts. We will present current models and propose alternative mechanisms allowing cells to spatially and temporally coordinate microtubule and mitotic spindle assembly.

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How to tune spindle size relative to cell size?

Cited by 7 publications

References 41 publications

Spatial variation of microtubule depolymerization in large asters

Spatial variation of microtubule depolymerization in large asters

Organelle size scaling over embryonic development

Spatial and Temporal Scaling of Microtubules and Mitotic Spindles

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