The Analysis of a Pseudoallelic Recessive Lethal System at the Notch Locus of Drosophila melanogaster

Notch2, but not Notch1, is required for proximal fate acquisition in the mammalian nephron

“…Thus, Notch1 is clearly non-essential for this process and Notch2 is the only ␥-secretase substrate that plays a significant role in these patterning events. As soon as Notch was identified as an X-linked locus in Drosophila (Welshons, 1958), it was realized that the wing phenotype associated with Notch mutations was due to haploinsufficiency. Notch1 is haploinsufficient in vertebrates as well: myelination in the mouse is slowed in Notch1 heterozygote animals (Givogri et al, 2002), and human tricuspid 809 RESEARCH ARTICLE Notch2 drives nephron segmentation heart valve development and maintenance of valve flexibility throughout adult life require both alleles of Notch1 (Garg et al, 2005).…”

Effect of temperature on interaction of Abruptex and recessive alleles of the Notch complex locus of Drosophila melanogaster

“…The expression of these alleles varied less with the temperature than that of hypermorphic alleles. AX"2 had on an average a weak .fir"" WELSHONS (1965WELSHONS ( , 1971, LINDSLEY and GRELL (1968), FOSTER (1979, PORTIN (1979, SHELLENBARGER and MOHLER (1975 expression at all temperatures, Ax'6172 had a clear expression at all temperatures, and Ax7Id had a clear expression at 18" and 25" and a somewhat stronger expression at 29". The expression of lethal Abruptex alleles varied strongly and clearly with the temperature.…”

“…A variety of temperature-sensitive lethal and morphological alleles are also known (HOUSE 1959;HILLMAN 1962;FOSTER and SUZUKI 1970;FOSTER 1973;SHELLEN-BARGER 1971;SHELLENBARGER and MOHLER 1975;PORTIN and SIREN 1976). In spite of the diverse pleiotropic developmental effects of the gene, and the intricate complementation pattern of its mutations, WELSHONS (1965) concluded that the Notch gene was a single cistron based on the fact that even though the lethal mutations are distributed throughout the locus, neither do they complement each other nor the recessive visible mutations. Although the Notch complex gene has been under intensive investigation for several decades, its primary function is still unknown.…”

“…Mutations at this locus range from embryonic lethals to recessive visible mutations affecting the eye or the wing (POULSON 1940;WELSHONS 1958aWELSHONS , 1965WELSHONS and VON HALLE 1962). A variety of temperature-sensitive lethal and morphological alleles are also known (HOUSE 1959;HILLMAN 1962;FOSTER and SUZUKI 1970;FOSTER 1973;SHELLEN-BARGER 1971;SHELLENBARGER and MOHLER 1975;PORTIN and SIREN 1976).…”

Endocytosis in Notch Signaling Activation

“…H . Morgan's laboratory about a century ago, as a dominant mutant with a peculiar toothed/notched wing margin in heterozygosity [56]; this phenotype was later associated with additional defects, including thickened wing veins, and bristle abnormalities [57]. In hemizygosity, or in homozygous females in flies, Notch loss-of-function mutations are embryonic lethal with neuralization of important parts of the ectoderm, leading to hypertrophy of the central nervous system and corresponding hypotrophy of the epidermis of the fully developed embryo [58,59].…”