The apical extracellular matrix (aECM) that overlies epithelial cells performs essential protective, structural, and physiological functions. Additionally, the aECM has recently been shown to be an important mediator of morphogenesis and development. We find that the aECM protein, FBN-1, is required to prevent the deformation of epidermal cells by several intrinsic biomechanical forces that arise during development. These forces include the actomyosin-based circumferential constriction that elongates the embryo and a previously uncharacterized force that pulls the anterior epidermis inwards. Using genetic analysis together with a FRET-based tension sensor, we demonstrate that resistance of the embryonic pharynx to elongation or stretch produces this inward pulling force, which depends on attachment of the pharynx to the anterior epidermis. FBN-1 is a zona pellucida domain protein that shares a number of structural features with vertebrate fibrillins, which have been implicated in several human diseases including Marfan syndrome. FBN-1 is both required and expressed in the embryonic epidermis and is secreted to the apical surface of epidermal cells where it functions as a putative component of the embryonic sheath. Correct processing of fbn-1 mRNA isoforms requires the conserved alternative splicing factor MEC-8/RBPMS. Loss of mec-8 leads to a pronounced change in the profile of fbn-1 mRNA isoforms, reduced FBN-1 activity, and a low penetrance of anterior morphogenesis defects. A parallel pathway that is likely to control aECM protein trafficking and secretion also promotes resistance of the epidermis to biomechanical forces. This pathway includes the conserved proteins SYM-3/FAM102A and SYM-4/WDR44, which likely function with the RAB-11 GTPase to promote the secretion of aECM components. Correspondingly, mutations in sym-3, sym-4, and rab-11 enhance mutations in mec-8 and fbn-1, and the compound mutants display severe morphological defects that result from deformation of the epidermis by mechanical forces. Our studies underscore the importance of the aECM in promoting normal morphogenesis and identify a network of genes required for the correct processing and localization of aECM components.
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