Four classes of alleles, all recessive.
(1) en1. Viable hemizygous and homozygous; fertile. Longitudinal cleft extends from rear border of scutellum forward,
may be reduced to median nick or posterior flattening of scutellum. Wings larger, broader, and thin textured with spatulate end; venation and distribution of sensilla abnormal in
posterior wing compartment. Variable duplication of anterior
triple row bristles on posterior margin; alula reduced, with
costal-like bristles. In males, extra sex comb often present
(Brasted, 1941, Genetics 26: 347-73), smaller than normal,
and in mirror-image position in posterior compartment. Duplications of transverse rows in female prothoracic leg, extra
bristles in mesothoracic and metathoracic tarsi (Garcia-Bellido, and Santamaria, 1972, Genetics 72: 87-104; Lawrence,
Struhl, and Morata, 1979, J. Embryol. Exp. Morph. 51: 195-208). Action of en1 is autonomous except for scutellar cleft
(Tokunaga, 1961, Genetics 46: 157-76; Stern and Tokunaga,
1968, Proc. Nat. Acad. Sci. USA 60: 1252-59; Garcia-Bellido,
and Santamaria, 1972, Genetics 72: 87-104). Clones of en
cells of posterior compartment origin fail to respect
anterior-posterior compartment border in wing disc as do mwh
clones in wing discs of en1 homozygotes (Morata and Lawrence,
1975, Nature 255: 614-17; Morata and Lawrence, 1976, Dev.
Biol. 50: 321-37). en abnormalities are associated with posterior compartment structures only, except for scutellar
cleft. Restriction of glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase (Cunninghamn, Smith, Makowski,
and Kuhn, 1983, Mol. Gen. Genet. 191: 238-43) and of a protein recognized by monoclonal antibody PS2 (Brower, 1984,
Nature 310: 496-98; 1987, EMBO J. 5: 2649-56) to posterior
compartment of wing disc altered by en1. Interaction with ci,
cg, sx (House, 1953, Genetics 38: 200-15; House, 1953,
Genetics 38: 309-27; House, 1961, Genetics 46: 871; Mukherjee, 1965, Genetics 51: 285-304; Datta and Mukherjee, 1971,
Genetics 68: 269-86) and fu (Fausto-Sterling and Smith-Schiess, 1982, EMBO J. 1: 827-33) partially increase phenotype. No suppression by su(Hw).
(2) Lethal alleles with normal cytology. Embryonic lethal.
Anterior margin of each segment defective. Pair rule defects
in naked cuticle of T1, T3, A2, A4, A6, A8 result in pair-wise
fusion of adjacent segments. Autonomous effects in adult
cuticular clones observed in posterior compartment of proboscis, thorax, abdomen, and genitalia. enlethal clones are
without effect in anterior compartments and in eye-antennal
region (Kornberg, 1981, Proc. Nat. Acad. Sci. USA 78: 1095-99; Kornberg, 1981, Dev. Biol. 86: 363-72; Lawrence and
Struhl, 1982, EMBO J. 1: 827-33). The en1/enlethal heterozygote characterized by wing abnormalities only; disruption of
anterior crossvein, gap in vein IV, and occasional socketted
bristles on posterior margin. In some combinations complementation is complete or nearly so (Condie and Brower, 1989, Dev.
Biol. 135: 31-42). No maternal effect (Lawrence, Johnston
and Struhl, 1983, Cell 35: 27-34).
(3) Deficiencies and lethal alleles with inversion or
translocation breakpoints. Embryonic lethal. Embryonic segment defects slight and variable. Alleles of this class in
heterozygous combination witn en1 produce adults more extreme
than en1. For example, in en1/en2, legs are truncated, the
tarsi reduced to densely bristled stumps; wings are greatly
enlarged and spatulate with greater disruption of veins IV and
V; higher penetrance of socketed bristles along the posterior
margin. Extreme scutellar cleft. At 29, duplication of anterior compartment bristles in mirror-image symmetry in posterior compartment of second antennal segment (Morata, Kornberg,
and Lawrence, 1983, Dev. Biol. 99: 27-33).
(4) Non-lethal alleles with breakpoints. Hemizygous viable,
embryos normal. Heterozygous with other allele classes, variable gaps in wing veins IV and V. Variable reductions or
deletions in male and female genitalia (Epper and Sanchez,
1983, Dev. Biol. 100: 387-98). Scutellum may also be