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Basal actomyosin pulses expand epithelium coordinating cell flattening and tissue elongation.

ABSTRACT: Actomyosin networks constrict cell area and junctions to alter cell and tissue shape. However, during cell expansion under mechanical stress, actomyosin networks are strengthened and polarized to relax stress. Thus, cells face a conflicting situation between the enhanced actomyosin contractile properties and the expansion behaviour of the cell or tissue. To address this paradoxical situation, we study late Drosophila oogenesis and reveal an unusual epithelial expansion wave behaviour. Mechanistically, Rac1 and Rho1 integrate basal pulsatile actomyosin networks with ruffles and focal adhesions to increase and then stabilize basal area of epithelial cells allowing their flattening and elongation. This epithelial expansion behaviour bridges cell changes to oocyte growth and extension, while oocyte growth in turn deforms the epithelium to drive cell spreading. Basal pulsatile actomyosin networks exhibit non-contractile mechanics, non-linear structures and F-actin/Myosin-II spatiotemporal signal separation, implicating unreported expanding properties. Biophysical modelling incorporating these expanding properties well simulates epithelial cell expansion waves. Our work thus highlights actomyosin expanding properties as a key mechanism driving tissue morphogenesis.

SUBMITTER: Li S

PROVIDER: S-EPMC11001887 | biostudies-literature | 2024 Apr

REPOSITORIES: biostudies-literature

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Basal actomyosin pulses expand epithelium coordinating cell flattening and tissue elongation.

Li Shun S Liu Zong-Yuan ZY Li Hao H Zhou Sijia S Liu Jiaying J Sun Ningwei N Yang Kai-Fu KF Dougados Vanessa V Mangeat Thomas T Belguise Karine K Feng Xi-Qiao XQ Liu Yiyao Y Wang Xiaobo X

Nature communications 20240408 1

Actomyosin networks constrict cell area and junctions to alter cell and tissue shape. However, during cell expansion under mechanical stress, actomyosin networks are strengthened and polarized to relax stress. Thus, cells face a conflicting situation between the enhanced actomyosin contractile properties and the expansion behaviour of the cell or tissue. To address this paradoxical situation, we study late Drosophila oogenesis and reveal an unusual epithelial expansion wave behaviour. Mechanisti ...[more]

PMID: 38589403

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Project description:Background and aimsThe precise control of brassinosteroid (BR) homeostasis and signalling is a prerequisite for hypocotyl cell elongation in plants. Arabidopsis MYB42 and its paralogue MYB85 were previously identified to be positive regulators of secondary cell wall formation during mature stages. Here, we aim to reveal the role of MYB42 and MYB85 in hypocotyl elongation during the seedling stage and clarify how MYB42 coordinates BR homeostasis and signalling to regulate this process.MethodsHistochemical analysis of proMYB42-GUS transgenic plants was used for determination of the MYB42 expression pattern. The MYB42, 85 overexpression, double mutant and some crossing lines were generated for phenotypic observation and transcriptome analysis. Transcription activation assays, quantitative PCR (qPCR), chromatin immunoprecipitation (ChIP)-qPCR and electrophoretic mobility shift assays (EMSAs) were conducted to determine the relationship of MYB42 and BRASSINAZOLE-RESISTANT 1 (BZR1), a master switch activating BR signalling.Key resultsMYB42 and MYB85 redundantly and negatively regulate hypocotyl cell elongation. They function in hypocotyl elongation by mediating BR signalling. MYB42 transcription was suppressed by BR treatment or in bzr1-1D (a gain-of-function mutant of BZR1), and mutation of both MYB42 and MYB85 enhanced the dwarf phenotype of the BR receptor mutant bri1-5. BZR1 directly repressed MYB42 expression in response to BR. Consistently, hypocotyl length of bzr1-1D was increased by simultaneous mutation of MYB42 and MYB85, but was reduced by overexpression of MYB42. Expression of a number of BR-regulated BZR1 (non-)targets associated with hypocotyl elongation was suppressed by MYB42, 85. Furthermore, MYB42 enlarged its action in BR signalling through feedback repression of BR accumulation and activation of DOGT1/UGT73C5, a BR-inactivating enzyme.ConclusionsMYB42 inhibits hypocotyl elongation by coordinating BR homeostasis and signalling during primary growth. The present study shows an MYB42, 85-mediated multilevel system that contributes to fine regulation of BR-induced hypocotyl elongation.

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Basal actomyosin pulses expand epithelium coordinating cell flattening and tissue elongation.

Publications

Basal actomyosin pulses expand epithelium coordinating cell flattening and tissue elongation.

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