sma-1 encodes a βH-spectrin homolog required for Caenorhabditis elegans morphogenesis

作者：Caroline R. McKeown, Vida Praitis, Judith Austin · 发表于：Development · 年份：1998 · DOI：10.1242/dev.125.11.2087 · 被引用次数：154 · 研究领域：Genetics, Aging, and Longevity in Model Organisms、Circadian rhythm and melatonin、Pluripotent Stem Cells Research

Morphogenesis transforms the C. elegans embryo from a ball of cells into a vermiform larva. During this transformation, the embryo increases fourfold in length; present data indicates this elongation results from contraction of the epidermal actin cytoskeleton. In sma-1 mutants, the extent of embryonic elongation is decreased and the resulting sma-1 larvae, although viable, are shorter than normal. We find that sma-1 mutants elongate for the same length of time as wild-type embryos, but at a decreased rate. The sma-1 mutants we have isolated vary in phenotypic severity, with the most severe alleles showing the greatest decrease in elongation rate. The sma-1 gene encodes a homolog of betaH-spectrin, a novel beta-spectrin isoform first identified in Drosophila. sma-1 RNA is expressed in epithelial tissues in the C. elegans embryo: in the embryonic epidermis at the start of morphogenesis and subsequently in the developing pharynx, intestine and excretory cell. In Drosophila, betaH-spectrin associates with the apical plasma membrane of epithelial cells; beta-spectrin is found at the lateral membrane. We propose that SMA-1 is a component of an apical membrane skeleton in the C. elegans embryonic epidermis that determines the rate of elongation during morphogenesis.