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Caballero-Mancebo, S.

Publications and source records attributed to Caballero-Mancebo, S..

3 recordsLinked to original sources

Spatiotemporal regulation of LGN/NuMA and astral microtubules generate mirror symmetric spindle rotations

The positioning of the mitotic spindle controls the size, content, and position of daughter cells within embryos and tissues. A major spindle positioning mechanism is cortical pulling whereby the membrane-bound complex LGN/NuMA/Dynein captures astral microtubules and pulls centrosomes toward the cell cortex. Cytoplasmic dynein and astral growth tend to counteract cortical pulling and position spindles at the cell center. It remains unclear how these opposing forces cooperate. Here we examine the ascidian embryo, where spindles of two germ line cells rotate toward one another causing divisions which are both mirror symmetric and unequal. We find that this spindle behavior is governed by transient enrichment of LGN and NuMA and enhanced cortical pulling at the shared cell contact. Inhibition of the LGN/NuMA complex disrupts spindle alignment, unequal cleavage, and mirror symmetry. Temporal analysis shows that cortical pulling force initates at anaphase when there is a sharp increase in astral microtubule length. These results point towards two phases of spindle positioning forces, with cytoplasmic pulling and cortical pulling operating sequentially during early and late mitosis.

cell biology↗

Mechanical forces in extendable tissue matrix orient cell divisions via microtubule stabilization in Arabidopsis

Plant morphogenesis relies exclusively on oriented cell expansion and division. Nonetheless, the mechanism(s) determining division plane orientation remain elusive. Here we studied tissue healing after laser-assisted wounding in roots and uncovered how mechanical forces of cell expansion stabilize and reorient microtubule cytoskeleton for orientation of cell division. We revealed that root tissue functions as interconnected cell matrix with a radial gradient of tissue extendibility causing a predictable tissue deformation after wounding. This causes instant redirection of expansion in the surrounding cells and reorientation of microtubule arrays ultimately predicting cell division orientation. Microtubules are destabilized under low tension, whereas stretching of cells, either through wounding or external aspiration immediately induce their polymerisation. The higher microtubule abundance in the stretched cell parts leads to reorientation microtubule arrays and ultimately cell division planes. This provides a long-sought mechanism for flexible re-arrangement of cell divisions by mechanical forces for tissue reconstruction and plant architecture.

cell biology↗

Tension-dependent stabilization of E-cadherin limits cell-cell contact expansion

Tension of the actomyosin cell cortex plays a key role in determining cell-cell contact growth and size. The level of cortical tension outside of the cell-cell contact, when pulling at the contact edge, scales with the total size to which a cell-cell contact can grow1,2. Here we show in zebrafish primary germ layer progenitor cells that this monotonic relationship only applies to a narrow range of cortical tension increase, and that above a critical threshold, contact size inversely scales with cortical tension. This switch from cortical tension increasing to decreasing progenitor cell-cell contact size is caused by cortical tension promoting E-cadherin anchoring to the actomyosin cytoskeleton, thereby increasing clustering and stability of E-cadherin at the contact. Once tension-mediated E-cadherin stabilization at the contact exceeds a critical threshold level, the rate by which the contact expands in response to pulling forces from the cortex sharply drops, leading to smaller contacts at physiologically relevant timescales of contact formation. Thus, the activity of cortical tension in expanding cell-cell contact size is limited by tension stabilizing E-cadherin-actin complexes at the contact.

cell biology↗