Proposed model linking zfPRL-3 function to YSL organization, epiboly dynamics, and embryonic outcomes. (A) In wild-type embryos, zfPRL-3 is proposed to prevent premature actomyosin ring formation and to maintain proper yolk syncytial layer (YSL) organization, including an organized F-actin structure and coherent distribution of YSL nuclei. This supports coordinated epiboly progression and subsequent normal morphogenesis. (B) In zfPRL-3 morphants, loss of zfPRL-3 is proposed to promote premature actomyosin ring formation and disrupt YSL organization, accompanied by dispersed YSL nuclei. These cellular-level alterations are associated with stalled epiboly and/or premature constriction, which can lead to yolk rupture and ultimately morphogenetic failure or embryonic death.
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