Abstract
The control of cell shape during cytokinesis requires a precise regulation of mechanical properties of the cell cortex. Only few studies have addressed the mechanisms underlying the robust production of unequal-sized daughters during asymmetric cell division. Here we report that unequal daughter-cell sizes resulting from asymmetric sensory organ precursor divisions in Drosophila are controlled by the relative amount of cortical branched Actin between the two cell poles. We demonstrate this by mistargeting the machinery for branched Actin dynamics using nanobodies and optogenetics. We can thereby engineer the cell shape with temporal precision and thus the daughter-cell size at different stages of cytokinesis. Most strikingly, inverting cortical Actin asymmetry causes an inversion of daughter-cell sizes. Our findings uncover the physical mechanism by which the sensory organ precursor mother cell controls relative daughter-cell size: polarized cortical Actin modulates the cortical bending rigidity to set the cell surface curvature, stabilize the division and ultimately lead to unequal daughter-cell size.
| Original language | English |
|---|---|
| Pages (from-to) | 235-245 |
| Number of pages | 11 |
| Journal | Nature Cell Biology |
| Volume | 25 |
| Issue number | 2 |
| DOIs | |
| Publication status | Published - 6 Feb 2023 |
Bibliographical note
Funding Information:This work has been supported by the Swiss National Science Foundation, the European Research Council, the NCCR Chemical Biology programme, the DIP of the Canton of Geneva and the SystemsX EpiPhysX (MGG). A.M. acknowledges support from an ELBE PhD fellowship, from an EMBO Longterm Fellowship (European Molecular Biology Organization, ALTF 528-2019) and from a DFG Postdoctoral Research Fellowship (Deutsche Forschungsgemeinschaft, Project 431144836), and F.J. was supported by the Cluster of Excellence Physics of Life, TU Dresden. In particular, we thank B. Baum, M. Fritzsche, Z. Hadjivasiliou and I. F. Sbalzarini for helpful discussions, K. Kruse, C. González, O. Afonso and M. Martinez Merino for critical reading of the manuscript, and J. Pampalona (from Cayetano González lab) and V. Sabado (from Emi Nagoshi lab) for training of the Drosophila neuroblast primary culture. We also thank M. Dubois for technical support and T. Lecuit, S. Bogdan, F. Payre, E. Moreno, P. N. Adler, F. Karch, A. Brand and M. Baylies for providing Drosophila fly lines, as well as Bloomington Drosophila Stock Center, Vienna Drosophila Resource Center and the Developmental Studies Hybridoma Bank for reagents.
Funding Information:
This work has been supported by the Swiss National Science Foundation, the European Research Council, the NCCR Chemical Biology programme, the DIP of the Canton of Geneva and the SystemsX EpiPhysX (MGG). A.M. acknowledges support from an ELBE PhD fellowship, from an EMBO Longterm Fellowship (European Molecular Biology Organization, ALTF 528-2019) and from a DFG Postdoctoral Research Fellowship (Deutsche Forschungsgemeinschaft, Project 431144836), and F.J. was supported by the Cluster of Excellence Physics of Life, TU Dresden. In particular, we thank B. Baum, M. Fritzsche, Z. Hadjivasiliou and I. F. Sbalzarini for helpful discussions, K. Kruse, C. González, O. Afonso and M. Martinez Merino for critical reading of the manuscript, and J. Pampalona (from Cayetano González lab) and V. Sabado (from Emi Nagoshi lab) for training of the Drosophila neuroblast primary culture. We also thank M. Dubois for technical support and T. Lecuit, S. Bogdan, F. Payre, E. Moreno, P. N. Adler, F. Karch, A. Brand and M. Baylies for providing Drosophila fly lines, as well as Bloomington Drosophila Stock Center, Vienna Drosophila Resource Center and the Developmental Studies Hybridoma Bank for reagents.
Publisher Copyright:
© 2023, The Author(s).
Keywords
- Actins
- Nuclear Family
- Cytokinesis
- Neurons
- Stem Cells