PubMed · 14263267
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E J AMBROSE. 1965. CELL MOVEMENTS.. https://doi.org/10.1016/0160-9327(65)90094-3
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Oncogenic mutations of the PIK3CA gene, which encodes the catalytic subunit of the phosphatidylinositol 3-kinase (PI3K) enhance cell migration via ERK (ERK1 and ERK2, also known as MAPK3 and MAPK1, respectively) activation. We analyzed the factors regulating collective cell migration (CCM) of genome-edited MCF10A cell lines carrying hotspot PIK3CA mutations E545K or H1047R. H1047R enhanced CCM and promoted the propagation of waves of ERK activity backwards from the wound edge, whereas E545K impaired both coordinated CCM and ERK activity wave formation. The distance traveled by ERK activity waves correlated with directional persistence of migrating cells. Inhibition of cell contractility stimulated ERK wave propagation and efficient CCM of E545K cells but impaired ERK waves and CCM in control cells. Impaired ERK wave propagation was consistently associated with non-linear cell-cell junctions and the loss of polarized distribution of actomyosin. Taken together, these analyses suggest that polarized actomyosin contractility and pulsatile ERK activation must be constrained in the territory of a phase diagram compatible with mechanotransduction of ERK waves across cell-cell junctions to achieve highly coordinated and efficient collective migration.
We have previously shown that human corneal epithelial cells respond to synthetic topographic features with dimensions similar to those found in the native human corneal basement membrane. Epithelial cells integrated inputs from substrate topography and soluble factors in the culture medium to generate alignment responses to substrate topographic anisotropies. Human keratocytes are the main cellular components of the stroma, the tissue that underlies the corneal epithelium. Here we report that keratocytes aligned more strongly than epithelial cells along topographic patterns of grooves and ridges. On patterns with pitches of 800 nm and larger approximately 70% of keratocytes were aligned along the patterns compared to 35% for epithelial cells. On 70 nm-wide ridges on a 400-nm pitch, keratocyte alignment dropped to 45%, whereas epithelial cell alignment remained constant. Similarly to epithelial cells, focal adhesions and associated stress fibers in keratocytes were aligned mainly along the substrate topographies, although oblique orientations were also observed. Furthermore, keratocytes cultured on the nanoscale patterns had fewer stress fibers and focal adhesions than cells cultured on microscale patterns or on smooth substrates.
The genetic and molecular bases of various types of congenital pigmentary disorders have been classified in the past 10 years, as follows: (1) disorders of melanoblast migration in the embryo from the neural crest to the skin: piebaldism; Waardenburg syndrome 1-4 (WS1-WS4); dyschromatosis symmetrica hereditaria. (2) Disorders of melanosome formation in the melanocyte: Hermansky-Pudlak syndrome 1-7 (HPS1-7); Chediak-Higashi syndrome 1 (CHS1). (3) Disorders of melanin synthesis in the melanosome: oculocutaneous albinism 1-4 (OCA1-4). (4) Disorders of mature melanosome transfer to the tips of the dendrites Griscelli syndrome 1-3 (GS1-3). These disorders are presented and their gene mutations and pathogenesis are discussed.