606B Poster - 08. Patterning, morphogenesis and organogenesis
Friday April 08, 2:00 PM - 4:00 PM

Authors:
Kimberley Gauthier ¹; Julie Brill ^1,2

Affiliations:
1) Cell Biology Program, The Hospital For Sick Hospital, Toronto, Canada; 2) Department of Molecular Genetics, University of Toronto, Toronto, Canada

Keywords:
q. epithelial sheets; a. cytoskeleton

A recurring theme throughout development and epithelial tissue morphogenesis is the sealing or fusion of epithelial tissues, forming new cell junctions and a single seamless layer of cells. This process is central in wound healing, and dysregulation can lead to developmental anomalies such as cleft palates and neural tube defects. Epithelial sealing is essential in dorsal closure during Drosophila embryogenesis in which the epidermis wraps around the developing embryo, covering the underlying epithelium (the amnioserosa) and rejoining at the dorsal midline where the tissue seamlessly zippers shut. Dorsal closure is driven by actomyosin contractility in the amnioserosa, Jun kinase (JNK) signaling in the leading edge cells of the epidermis, and formation of a supracellular actin cable around the dorsal hole. Previously, embryos with Sac1 mutations were found to die during embryogenesis, leaving behind gaping dorsal anterior holes. Sac1 is a lipid phosphatase that dephosphorylates phosphatidylinositol-4-phosphate (PI4P), a lipid needed for membrane trafficking from the Golgi. Sac1 mutant embryos also have ectopic JNK activation and excessive cellular constriction in the amnioserosa. How Sac1 regulates JNK signaling and actomyosin contractility during dorsal closure remains unknown. Using time-lapse confocal microscopy to image a fluorescent myosin regulatory light chain marker, I found that dorsal closure proceeds at a slower pace in Sac1 mutants, and that some embryos develop tears in the amnioserosa and epidermal puckering towards the final stages of dorsal closure. In ongoing studies, I will further characterize the role of Sac1 in regulating epithelial sealing, actomyosin contractility, and JNK signaling activation. My results will uncover how Sac1 and phospholipid homeostasis orchestrate contractile forces and cellular signaling to promote tissue morphogenesis.