Coronin 1A depletion restores the nuclear stability and viability of Aip1/Wdr1-deficient neutrophils
- Bowes, C., Redd, M., Yousfi, M., Tauzin, M., Murayama, E., Herbomel, P.
- The Journal of cell biology 218(10): 3258-3271 (Journal)
- Registered Authors
- Bowes, Charnese, Herbomel, Philippe, Murayama, Emi, Redd, Michael, Tauzin, Muriel, Yousfi, Malika
- MeSH Terms
- 4-Butyrolactone/analogs & derivatives*
- Cell Nucleus/metabolism*
- Cell Survival
- Microfilament Proteins/deficiency*
- 31471458 Full text @ J. Cell Biol.
Bowes, C., Redd, M., Yousfi, M., Tauzin, M., Murayama, E., Herbomel, P. (2019) Coronin 1A depletion restores the nuclear stability and viability of Aip1/Wdr1-deficient neutrophils. The Journal of cell biology. 218(10):3258-3271.
Actin dynamics is central for cells, and especially for the fast-moving leukocytes. The severing of actin filaments is mainly achieved by cofilin, assisted by Aip1/Wdr1 and coronins. We found that in Wdr1-deficient zebrafish embryos, neutrophils display F-actin cytoplasmic aggregates and a complete spatial uncoupling of phospho-myosin from F-actin. They then undergo an unprecedented gradual disorganization of their nucleus followed by eruptive cell death. Their cofilin is mostly unphosphorylated and associated with F-actin, thus likely outcompeting myosin for F-actin binding. Myosin inhibition reproduces in WT embryos the nuclear instability and eruptive death of neutrophils seen in Wdr1-deficient embryos. Strikingly, depletion of the main coronin of leukocytes, coronin 1A, fully restores the cortical location of F-actin, nuclear integrity, viability, and mobility of Wdr1-deficient neutrophils in vivo. Our study points to an essential role of actomyosin contractility in maintaining the integrity of the nucleus of neutrophils and a new twist in the interplay of cofilin, Wdr1, and coronin in regulating F-actin dynamics.
Genes / Markers
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Engineered Foreign Genes