Essential for the development of polarized epithelia, for cell polarity associated with asymmetric cell division of neuroblasts during development, and for oocyte polarity formation. Promotes the formation of actin-rich projections at the oocyte cortex and the posterior enrichment of par-1 which is required for oocyte polarization. Regulates the localization of axis-specifying morphogens such as stau and grk.

(UniProt, P08111)

Homozygotes undergo embryogenesis and the first three larval instars; larvae reach normal maximum size; then for some alleles most homozygotes fail to pupate, becoming bloated and 1.5-2 times normal size, whereas for others the majority form prepupae but fail to progress into morphogenesis. Ring gland small and appears immature in third-instar larvae (Scharrer and Hadorn, 1938, Proc. Nat. Acad. Sci. USA 24: 236-42); third-instar l(2)gl larvae implanted with a normal ring gland pupate but do not metamorphose; injection of ecdysone elicits the same result (Karlson and Hanser, 1952, Z. Naturforsch 76: 80-83); thus a deficiency of hormones from the ring gland is probably one, but not the only, result of l(2)gl. Homozygotes that die as prepupae have underdeveloped corpora allata and prothoracic glands, whereas larval lethals have underdeveloped prothoracic glands but normal corpora allata (Korochkina and Nazarova, 1977, Chromosoma 62: 175-90). Prothoracic glands contain approximately 1% the normal quantity of smooth endoplasmic reticulum (Aggarwal and King, 1969, J. Morph. 129: 171-99). Alleles range from 98% larval and 2% pupal death to 18% larval and 82% pupal death (Gateff, Golubovsky, and Sokolova, 1977, DIS 52: 128-29). In the most extreme phenotypes (+++), the larval brain and optic lobes become enlarged and disorganized and the imaginal discs large and clumped; when discs of such larvae are transplanted into wild-type-female abdomens, they form large contained tumors, whereas transplanted optic primordia from larval brains form invasive neuroblastomas, which grow rapidly, killing the host within 7-14 days; they can be serially cultured in adult abdomens (Gateff and Schneiderman, 1974). These observations have led to l(2)gl's being designated a Drosophila oncogene. Intermediate alleles (++) exhibit moderately enlarged brain and discs, which show enhanced growth when transplanted into wild-type females and death of host is delayed. In weak alleles (+) the brain and discs are small and rudimentary and grow slowly in transplants. One allele normal in disc morphology and behavior in transplants (-). The lethal phase is not well correlated with the phenotypic expression. Most abundant transcription noted in early (0-6 h) embryos and late third-instar larvae, with the smaller transcript more abundant in embryos and the larger in larvae (Mechler, McGinnis, and Gehring). Immunocytochemistry shows localization of l(2)gl product at cell surfaces, specifically at the interfaces between proliferating cells (Klambt and Schmidt, 1986, EMBO J. 5: 2955-61; Klambt, Muller, Lutzelschwab, Rossa, Totzke, and Schmidt, 1989, Dev. Biol. 133: 425-36; Lutzelschwab, Klambt, Rossa, and Schmidt, 1987, EMBO J. 6: 1791-97). During later embryogenesis relatively high amounts of l(2)gl protein is detected in pole cells and cells of the developing nervous system; specifically neurons in the peripheral nervous system undergoing axogenesis express the protein. Monoclonal antibodies specifically stain junctions between mammalian cells in culture as though they are recognizing either membrane or intercellular-matrix proteins (Klambt et al., 1989). Ten-to-eleven-day-old larvae homozygous for larval-lethal alleles exhibit remarkably few puff sites, only 63BC and occasionally 88D and 89B; however, heat shock induced puffs develop normally (Ashburner, 1970, Chromosoma 31: 356-76). Homozygotes able to form prepupae exhibit more nearly normal puffing patterns; puffing in response to administration of ecdysone also appears normal (Richards, 1976, Wilhelm Roux's Arch. Dev. Biol. 179: 339-48).