Zimm, G.G. and D.L Lindsley. Department of Biology, University of
California, San Diego, La Jolla, CA 92093-0322.
Upturned revisited with description of a new allele.
Among the progeny of phenotypically wild-type males treated with ethyl
methanesulfonate, one fly with curly wings was recovered; the phenotype was
subsequently inherited as a dominant mutation that segregated with
chromosome 2; crossing over with al b c px sp was normal, and no
straight-winged recombinants with c (2-75.5) were recovered among 161
testcross progeny. This result places the new mutation in the vicinity of
Upturned (U). The allele U1 is associated with a pericentric inversion
with breakpoints at 40F and 53A according to Bridges and Li (Morgan,
Bridges, and Schultz, 1935). The genetic map position originally given for
U was 70+/- based on the mapping of a putative second allele, UH20,
isolated by Tanaka (1937); more recently Ashburner has revised this
position to 2-76, based on the 53A breakpoint of In(2LR)U1, (FlyBase,
1994). In(2LR)U1 is homozygous lethal, and UH20, now lost, was
homozygous viable. The new mutation is also homozygous lethal, but it
survives in heterozygous combination with U1. If the new mutation is an
allele of U, then at least one of the above two is not a lethal allele. To
clarify this ambiguity, we generated an X-ray-induced revertant of U1 and
found that it is lethal in combination with the new mutant; thus we
conclude that the new mutation is a lethal allele of U, whereas U1 is a
viable allele with a lethal mutation elsewhere on the chromosome; we
designate the new allele U2. U1/U2, U1/Cy , and U2/Cy flies
show an additive effect of the curly-wing phenotype.
We have been unsuccessful in finding a deficiency that uncovers the
lethality of U2. The fact that neither four deficiencies for c at 52D1-7
(Saxton, pers. comm.; FlyBase, 1994) extend far enough to the right to
include 53A, coupled with our inability to establish stocks of nearly all
Xray-induced revertants of either U1 or U2, implies the existence of
haplo-insufficiency that is coincident with or closely linked to Upturned.
No duplications are available to cover the 53A1 breakpoint of In(2LR)U1.
The viability of U1 over Df(2L)C', a deficiency for the 2L
heterochromatin (Hilliker and Holm, 1975), indicates that the lethal
mutation in In(2LR)U1 is not associated with the breakpoint at 40F.
We were unable to cover the lethality of U1 in male homozygotes with
Dp(2;Y)G, a duplication that includes the 40F salivary region.
In our hands U1 (but not U2) exhibits reduced penetrance, with its
expression depending on genetic background and in general being less
reliable in males than in females. In the original description (Bridges,
1935), U1 was said to cause, in addition to upwardly curled wings,
crossed posterior scutellar bristles, darker than normal body color with
dark waxy wings, and eyes mottled with light flecks. Of these phenotypes
only upturned wings, crossed posterior scutellars, and darker than normal
body color are currently observed in U1 and U2 heterozygotes and
U1/U2 heteroalleles. Since U1 is associated with a pericentric
inversion with one break in proximal 2L heterochromatin, we speculated that
perhaps U1 was originally recovered in combination with a lt-bearing
homologue and that the eye mottling was variegation associated with removal
of the lt locus from its normal heterochromatic to a distal euchromatic
environment in In(2LR)U1; U1/lt flies exhibit variegated eyes in
addition to upturned wings, crossed postscutellar bristles, and darker body
color.
References:
Bridges, 1935, DIS 3: 5-19;
Bridges, 1937, DIS 7: 5-17;
Davis and MacIntyre, 1988, Genetics 120: 755-66;
FlyBase, 1994, Nucleic Acids Res. 22: 3456-58;
Hilliker and Holm, 1975, Genetics 81: 905-21;
Morgan et al., 1935-36 , Year Book - Carnegie Inst. Washington  35:289-97 ;
Saxton, pers. comm.;
Tanaka, 1937, DIS 8: 11.