Epiboly generates the epidermal basal monolayer and spreads the nascent mammalian skin to enclose the embryonic body

TY - JOUR

T1 - Epiboly generates the epidermal basal monolayer and spreads the nascent mammalian skin to enclose the embryonic body

AU - Panousopoulou, Eleni

AU - Hobbs, Carl

AU - Mason, Ivor

AU - Green, Jeremy B. A.

AU - Formstone, Caroline J.

PY - 2016/5/1

Y1 - 2016/5/1

N2 - Epiboly is a morphogenetic process that is employed in the surface ectoderm of anamniotes during gastrulation to cover the entire embryo. We propose here that mammals also utilise this process to expand the epidermis and enclose the body cavity and spinal cord with a protective surface covering. Our data supports a model whereby epidermal spreading is driven by the primary establishment of the epidermal basal progenitor monolayer via radial cell intercalation of a multi-layered epithelium towards the basal lamina. By using a suspension organotypic culture strategy we find that this process is fibronectin-dependent and autonomous to the skin. The radial cell rearrangements that drive epidermal spreading also require ROCK activity but are driven by cell protrusions and not myosin II contractility. Epidermal progenitor monolayer formation and epidermal spreading are delayed in Crash mice which possess a dominant mutation of Celsr1, an orthologue of the core planar-cell-polarity (PCP) protein Flamingo (Fmi). We observe a failure of ventral enclosure in Crash mutants suggesting that defective epidermal spreading might underlie some ventral wall birth defects.

AB - Epiboly is a morphogenetic process that is employed in the surface ectoderm of anamniotes during gastrulation to cover the entire embryo. We propose here that mammals also utilise this process to expand the epidermis and enclose the body cavity and spinal cord with a protective surface covering. Our data supports a model whereby epidermal spreading is driven by the primary establishment of the epidermal basal progenitor monolayer via radial cell intercalation of a multi-layered epithelium towards the basal lamina. By using a suspension organotypic culture strategy we find that this process is fibronectin-dependent and autonomous to the skin. The radial cell rearrangements that drive epidermal spreading also require ROCK activity but are driven by cell protrusions and not myosin II contractility. Epidermal progenitor monolayer formation and epidermal spreading are delayed in Crash mice which possess a dominant mutation of Celsr1, an orthologue of the core planar-cell-polarity (PCP) protein Flamingo (Fmi). We observe a failure of ventral enclosure in Crash mutants suggesting that defective epidermal spreading might underlie some ventral wall birth defects.

KW - Developmental biology

U2 - 10.1242/jcs.180703

DO - 10.1242/jcs.180703

M3 - Article

SN - 0021-9533

VL - 129

SP - 1915

EP - 1927

JO - Journal of Cell Science

JF - Journal of Cell Science

IS - 9

ER -