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The role of gliotactin in the formation of Drosophila septate junctions Schulte, Joost

Abstract

Gliotactin is a non-catalytically active, serinesterase-like, transmembrane protein that is required for the formation of the blood-nerve barrier in Drosophila. Gliotactin is expressed by the peripheral nervous system glia, which ensheath motor and sensory axons. Pleated septate junctions present between the wraps of peripheral glia have previously been shown to be required for blood-nerve barrier formation, and are believed to have a role in cell-cell adhesion. In gliotactin mutants, peripheral glia display wrapping defects at the distal reaches of embryonic peripheral nerves. Paralysis and death occurs in gliotactin mutants, as the disrupted blood-nerve barrier exposes neurons to the high potassium concentration of the haemolymph which causes action potential blockade. It has been hypothesized that the blood-nerve barrier and ensheathment phenotypes observed in gliotactin mutants arises from abnormal pleated septate junction development, or from a defect in other cellular events during peripheral glial development. Here, the role of Gliotactin in Drosophila pleated septate junction development was investigated. Through mutant analysis and cell biological techniques, it was found that Gliotactin is necessary for septate junction development, yet has a role that is unique from other previously identified pleated septate junction proteins. In addition to being expressed in the peripheral nervous system glia, Gliotactin was also found to be expressed in the epidermis, salivary glands, and a variety of other pleated septate junction containing tissues. Gliotactin in the epidermis and salivary glands is found concentrated at regions where three cells meet and is only partially overlapping with other septate junction proteins. At these tricellular junctions, Gliotactin physically associates with septate junction proteins, as demonstrated through co-immunoprecipitation experiments. Through dye injection assays, it was demonstrated that loss of Gliotactin results in the disruption of the integrity of the transepithelial barrier in the salivary gland, similar to other pleated septate junction mutants. A model is proposed in which Gliotactin at tricellular corners acts as a physical link between pleated septate junctions and specialized structures, termed tricellular plugs which have previously been identified at tricellular junctions.

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