細(xì)胞運動的接觸抑制現(xiàn)象,，是超過50年前首次在體外成纖維細(xì)胞中被發(fā)現(xiàn)的，研究人員認(rèn)為,，有缺陷的接觸抑制是惡性細(xì)胞入侵中的一個因素。該現(xiàn)象是當(dāng)兩個細(xì)胞接觸時出現(xiàn)的：它們會將其伸出的部分收回，并改變自己的運動方向,。但這種抑制的分子基礎(chǔ)、以及它是否也在活體出現(xiàn)仍然是存在爭議的問題,。
現(xiàn)在,，神經(jīng)冠細(xì)胞（起源于胚胎的高遷移性細(xì)胞）的延時顯微技術(shù)被用來在活體及體外演示運動的接觸抑制，而且它可以解釋它們的定向遷移,。但當(dāng)一個神經(jīng)冠細(xì)胞與另一個細(xì)胞類型相遇時,，它卻沒有顯示運動的接觸抑制，而是允許它入侵組織,。（生物谷Bioon.com）
生物谷推薦原始出處：
Nature 456, 957-961 (18 December 2008) | doi:10.1038/nature07441
Contact inhibition of locomotion in vivo controls neural crest directional migration
Carlos Carmona-Fontaine1, Helen K. Matthews1, Sei Kuriyama1, Mauricio Moreno1, Graham A. Dunn2, Maddy Parsons2, Claudio D. Stern1 & Roberto Mayor1
1 Department of Anatomy and Developmental Biology, University College London, London WC1E 6BT, UK
2 Randall Division of Cell and Molecular Biophysics, King's College London, London SE1 1UL, UK
Top of pageContact inhibition of locomotion was discovered by Abercrombie more than 50 years ago and describes the behaviour of fibroblast cells confronting each other in vitro, where they retract their protrusions and change direction on contact1, 2. Its failure was suggested to contribute to malignant invasion3, 4, 5, 6. However, the molecular basis of contact inhibition of locomotion and whether it also occurs in vivo are still unknown. Here we show that neural crest cells, a highly migratory and multipotent embryonic cell population, whose behaviour has been likened to malignant invasion6, 7, 8, demonstrate contact inhibition of locomotion both in vivo and in vitro, and that this accounts for their directional migration. When two migrating neural crest cells meet, they stop, collapse their protrusions and change direction. In contrast, when a neural crest cell meets another cell type, it fails to display contact inhibition of locomotion; instead, it invades the other tissue, in the same manner as metastatic cancer cells3, 5, 9. We show that inhibition of non-canonical Wnt signalling abolishes both contact inhibition of locomotion and the directionality of neural crest migration. Wnt-signalling members localize at the site of cell contact, leading to activation of RhoA in this region. These results provide the first example of contact inhibition of locomotion in vivo, provide an explanation for coherent directional migration of groups of cells and establish a previously unknown role for non-canonical Wnt signalling.
