Forces drive basement membrane invasion in Caenorhabditis elegans

被引:27
作者
Caceres, Rodrigo [1 ,2 ,3 ]
Bojanala, Nagagireesh [1 ,3 ]
Kelley, Laura C. [4 ]
Dreier, Jes [5 ]
Manzi, John [1 ,3 ]
Di Federico, Fahima [1 ,3 ]
Chi, Qiuyi [4 ]
Risler, Thomas [1 ,3 ]
Testa, Ilaria [5 ]
Sherwood, David R. [4 ]
Plastino, Julie [1 ,3 ]
机构
[1] PSL Res Univ, CNRS, Lab Physicochim Curie, Inst Curie, F-75005 Paris, France
[2] Univ Paris 05, F-75005 Paris, France
[3] Sorbonne Univ, F-75005 Paris, France
[4] Duke Univ, Dept Biol, Regenerat Next, Durham, NC 27705 USA
[5] KTH Royal Inst Technol, Dept Appl Phys & Sci Life Lab, S-10014 Stockholm, Sweden
基金
欧洲研究理事会;
关键词
actin cytoskeleton; force production; cell invasion; Arp2/3; complex; anchor cell; ALDRICH-SYNDROME PROTEIN; ANCHOR-CELL INVASION; ARP2/3; COMPLEX; IN-VIVO; C; ELEGANS; INVADOPODIUM FORMATION; MOLECULAR-MECHANISMS; ACTIN; MIGRATION; WASP;
D O I
10.1073/pnas.1808760115
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
During invasion, cells breach basement membrane (BM) barriers with actin-rich protrusions. It remains unclear, however, whether actin polymerization applies pushing forces to help break through BM, or whether actin filaments play a passive role as scaffolding for targeting invasive machinery. Here, using the developmental event of anchor cell (AC) invasion in Caenorhabditis elegans, we observe that the AC deforms the BM and underlying tissue just before invasion, exerting forces in the tens of nanonewtons range. Deformation is driven by actin polymerization nucleated by the Arp2/3 complex and its activators, whereas formins and cross-inkers are dispensable. Delays in invasion upon actin regulator loss are not caused by defects in AC polarity, trafficking, or secretion, as appropriate markers are correctly localized in the AC even when actin is reduced and invasion is disrupted. Overall force production emerges from this study as one of the main tools that invading cells use to promote BM disruption in C. elegans.
引用
收藏
页码:11537 / 11542
页数:6
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