DRhoGEF2 Regulates Cellular Tension and Cell Pulsations in the Amnioserosa during Drosophila Dorsal Closure

被引:37
作者
Azevedo, Dulce [1 ]
Antunes, Marco [1 ]
Prag, Soren [1 ]
Ma, Xiaoyan [2 ]
Hacker, Udo [3 ]
Brodland, G. Wayne [4 ]
Hutson, M. Shane [2 ]
Solon, Jerome [5 ]
Jacinto, Antonio [1 ,6 ]
机构
[1] Univ Lisbon, Fac Med, Inst Mol Med, Lisbon, Portugal
[2] Vanderbilt Univ, Dept Phys & Astron, Vanderbilt Inst Integrat Biosyst Res & Educ, Nashville, TN 37235 USA
[3] Lund Univ, Lund Strateg Res Ctr Stem Cell Biol & Cell Therap, Dept Expt Med Sci, Lund, Sweden
[4] Univ Waterloo, Dept Civil & Environm Engn, Waterloo, ON N2L 3G1, Canada
[5] CRG Ctr Genom Regulat, Barcelona, Spain
[6] Inst Gulbenkian Ciencias, Oeiras, Portugal
来源
PLOS ONE | 2011年 / 6卷 / 09期
基金
欧洲研究理事会;
关键词
ADHERENS JUNCTIONS; APICAL CONSTRICTION; SHAPE CHANGES; ACTIN; MYOSIN; FORCES; CONTRACTILITY; MORPHOGENESIS; GASTRULATION; INVAGINATION;
D O I
10.1371/journal.pone.0023964
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Coordination of apical constriction in epithelial sheets is a fundamental process during embryogenesis. Here, we show that DRhoGEF2 is a key regulator of apical pulsation and constriction of amnioserosal cells during Drosophila dorsal closure. Amnioserosal cells mutant for DRhoGEF2 exhibit a consistent decrease in amnioserosa pulsations whereas overexpression of DRhoGEF2 in this tissue leads to an increase in the contraction time of pulsations. We probed the physical properties of the amnioserosa to show that the average tension in DRhoGEF2 mutant cells is lower than wild-type and that overexpression of DRhoGEF2 results in a tissue that is more solid-like than wild-type. We also observe that in the DRhoGEF2 overexpressing cells there is a dramatic increase of apical actomyosin coalescence that can contribute to the generation of more contractile forces, leading to amnioserosal cells with smaller apical surface than wild-type. Conversely, in DRhoGEF2 mutants, the apical actomyosin coalescence is impaired. These results identify DRhoGEF2 as an upstream regulator of the actomyosin contractile machinery that drives amnioserosa cells pulsations and apical constriction.
引用
收藏
页数:11
相关论文
共 28 条
  • [1] DRhoGEF2 regulates actin organization and contractility in the Drosophila blastoderm embryo
    Barmchi, MP
    Rogers, S
    Häcker, U
    [J]. JOURNAL OF CELL BIOLOGY, 2005, 168 (04) : 575 - 585
  • [2] The rho GTPase and a putative RhoGEF mediate a signaling pathway for the cell shape changes in Drosophila gastrulation
    Barrett, K
    Leptin, M
    Settleman, J
    [J]. CELL, 1997, 91 (07) : 905 - 915
  • [3] Cytoskeletal dynamics and supracellular organisation of cell shape fluctuations during dorsal closure
    Blanchard, Guy B.
    Murugesu, Sughashini
    Adams, Richard J.
    Martinez-Arias, Alfonso
    Gorfinkiel, Nicole
    [J]. DEVELOPMENT, 2010, 137 (16): : 2743 - 2752
  • [4] BRAND AH, 1993, DEVELOPMENT, V118, P401
  • [5] Genetic Screen in Drosophila melanogaster Uncovers a Novel Set of Genes Required for Embryonic Epithelial Repair
    Campos, Isabel
    Geiger, Jennifer A.
    Santos, Ana Catarina
    Carlos, Vanessa
    Jacinto, Antonio
    [J]. GENETICS, 2010, 184 (01) : 129 - U239
  • [6] Chou TB, 1996, GENETICS, V144, P1673
  • [7] The PAR complex regulates pulsed actomyosin contractions during amnioserosa apical constriction in Drosophila
    David, Daryl J. V.
    Tishkina, Alisa
    Harris, Tony J. C.
    [J]. DEVELOPMENT, 2010, 137 (10): : 1645 - 1655
  • [8] Scaling the microrheology of living cells
    Fabry, B
    Maksym, GN
    Butler, JP
    Glogauer, M
    Navajas, D
    Fredberg, JJ
    [J]. PHYSICAL REVIEW LETTERS, 2001, 87 (14) : 148102/1 - 148102/4
  • [9] Nonmuscle myosin II generates forces that transmit tension and drive contraction in multiple tissues during dorsal closure
    Franke, JD
    Montague, RA
    Kiehart, DP
    [J]. CURRENT BIOLOGY, 2005, 15 (24) : 2208 - 2221
  • [10] Can 1000 reviews be wrong?: Actin, α-catenin, and adherens junctions
    Gates, J
    Peifer, M
    [J]. CELL, 2005, 123 (05) : 769 - 772