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recessive.
i: see E(B)
I: see E(B)
Ic D: see bwVD
I-f: see E(f)
Idh: Isocitrate dehydrogenase
iab: see BXC
iav: inactive (J.C. Hall)
1
1
location: 1-18.8 (iav ), 20.7 (hypoB ).
synonym: hypoB.
references: Kaplan, 1977, DIS 52: 1.
Homyk and Sheppard, 1977, Genetics 87: 95-104.
Homyk, 1977, Genetics 87: 105-28.
O’Dell and Burnet, 1986, DIS 63: 107-08.
O’Dell, Coulon, David, Papin, Fuzeau-Braesch, and Jallon,
1977, Comptes Rendus Ser. III 305: 199-202.
O’Dell and Burnet, 1988, Heredity 61: 199-207.
O’Dell, Burnet, and Jallon, 1989, Heredity 62: 373-81.
1
phenotype: iav noted (Kaplan, 1977) to be extremely
inactive as adult, with normal external morphology;
population of mutants remains quiet and spread out evenly
in a container; will walk or fly when container disturbed,
2
but settles into inactivity soon afterward. iav noted
(Homyk and Sheppard, 1977) to be inactive and difficult to
arouse for flight (and, when it does, seems to hover and
fixate on objects); to jump and fly abnormally short
distances; to exhibit slow running or climbing ability and
optomotor response; to be debilitated after mechanical
shock (especially in adults more than two weeks old).
2
Gynandromorph analysis of iav
adult behavioral
impairments suggests primary focus could be neural
1
2
(Homyk, 1977). Open-field activity tests of iav and iav
(O’Dell and Burnet, 1988) showed both to exhibit reduced
speed as well as amount of locomotion (the former meaning
number of squares in the activity chambered visited/unit
time, the latter the proportion of time spent moving); male
activity levels higher than for females (also found for
wild-type); lower than wild-type levels of activity at all
ages between time of eclosion and approximately
one-month; yet, unlike wild type, speed and amount of
2
activity increase (in tests of iav ) in parallel between days 1
and 2 of adulthood (reaching a much lower than normal
1
2
plateau). In tests of homozygous iav and iav females
(with normal males), mating propensity reduced and
courtship durations extended, though such females showed
normal compositions of cuticular hydrocarbons and were
highly attractive to courting males (O’Dell et al., 1989);
mutant males with normal females exhibited slightly
reduced mating success; mutant males crossed with mutant
females had very low mating success rate. Lower than
normal octopamine levels, especially in extracts from adult
heads (O’Dell et al., 1987), with dopamine and
norepinephrine levels apparently normal.
1
2
3
alleles: iav , spontaneous (Kaplan, 1977), iav , iav , induced
1-3
by ethyl methanesulfonate [originally hypoB
(Homyk
and Sheppard, 1977)].
1
1
other information: Allelism of iav to hypoB shown by
O’Dell and Burnet (1986) in open field tests of
heterozygotes; they also note that both mutations are
location: 3-25.4 [based on Ohnishi and Voelkers mapping of
F
S
Idh vs Idh to a position between jv and se (1982, DIS
58: 121); Fox (1970, DIS 45: 35) mapped same
alternatives to 27.1].
3-27.2 [based on Bentley, Meidinger, and Williamson’s
nGB1
(1983, Biochem. Genet. 21: 725-33) mapping of Idh
+
vs Idh to a position between h and th].
synonym: Idh-NADP.
references: Fox, D.J., 1971, Biochem. Genet. 5: 69-80.
Williamson, Krochko, and Bentley, 1980, Comp. Biochem.
Physiol. 65B: 339-43.
Kuhn and Cunningham, 1986, Dev. Genet. 7: 21-34.
phenotype: Term for the structural gene or genes for
+
NADP -dependent
isocitrate
dehydrogenase
+
[threo-D-isocitrate:
NADP
oxydoreductase
(decarboxylating)];[IDH(E.C 1.1.1.42)]. Studies of purified
enzyme (Williamson) indicate it to have a molecular weight
of 110,000 and to be a dimer of subunits with molecular
weights 60,000 and 50,000. Whether these are products of
one or of two closely linked genes is uncertain; formation
F
S
of a hybrid dimer in Idh /Idh heterozygotes suggests a
single locus, but the mapping results outlined above are
suggestive of two. Only maternally derived enzyme
present during most of embryogenesis with vigorous
zygotic production beginning just prior to hatching (Wright
and Shaw, 1970, Biochem. Genet. 4: 385-94); peak activity
reached in third larval instar after which the level falls until
just prior to eclosion when it rises once more (Fox, 1971,
Biochem. Genet. 5: 69-80). Activity found in all tissues,
but especially high in larval fatbody and the sperm pump of
adult males and to a lesser extent in the larval and adult
midgut and the seminal recepticle and spermathecae (Fox,
Conscience-Egli, and Ab acherli, 1972, Biochem. Genet.
7: 163-75). Staining activity distributed nonuniformly in
the following imaginal discs: eye-antenna, all thoracic
discs, and genital, plus in larval gut, adult ovaries, and
internal male genitalia. Staining patterns formed gradually
in eye-antennal and wing disks. IDH staining pattern and
intensity changed in third instar larvae as ommatidia are
differentiated. When the tissue type is transformed by
homeotic genes, the IDH pattern is altered in a specific way
(Kuhn and Cunningham, 1986). Labial discs, histoblasts,
and salivary glands stain uniformly; clypeus-labrum disc,
imaginal foregut cells and imaginal ring of hind gut show
no activity (Cunningham and Kuhn, 1981, Insect Biochem.
11: 277-85).
phenotype
allele
synonym
ref 
IdhF
IdhnGB1
Idh6
3, 4
IdhnGB2
IdhnNC1
IdhGB2
residual
activity
heterodimer
formation
2, 6, 7
0
+
1, 2, 6, 7
5% 
-
2, 6, 7
0
+
S
Idh
SS
Idh
4
Idh
2
Idh
3, 4
Further descriptions below.
5
cytology: Located in 15A1-5 by in situ hybridization of
cloned DNA (Bogaert et al., 1987).
molecular biology: The gene encoding the PS2 -subunit
has been cloned, genomic and cDNA sequences obtained
(Bogaert et al., 1987). The predicted N terminus of the PS2
-subunit is part of a 4182-bp open reading frame that
encodes a 1394 amino acid protein of 154 kd; the
Drosophila N-terminal sequences show identity to the
sequences of both the heavy and light chains of -subunits
of the vertebrate fibronectin receptor family (Bogaert et al.,
1987; Leptin et al., 1987). The C-terminal region of the
Drosophila -subunit that shows no identity to the
vertebrate -subunit is characterized by the presence of
multiple serine repeats.

1 = Bentley, Meidinger, and Williamson, 1983, Biochem. Genet.
21: 725-33; 2 = Burkhart, Montgomery, Langley, and Voelker, 1984,
Genetics 107: 295-306; 3 = Fox, 1970, DIS 45: 35; 4 = Fox, 1971,
Biochem. Genet. 5: 69-80; 5 = Fox, 1972, DIS 48: 20; 6 = Langley,
Voelker, Leigh Brown, Ohnishi, Dickson, and Montgomery, 1981,
Genetics 99: 151-56; 7 = Voelker, Langley, Leigh Brown, Ohnishi,
Dickson, and Montgomery, and Smith, 1980 Proc. Nat. Acad. USA
77: 1091-95.

24% wild-type levels of CRM; kinetic properties of residual activity
indistinguishable from those of wild type.
cytology: Placed in region 66B-D by Voelker and Ohnishi
(Burkhardt, Montgomery, Langley and Voelker, 1984,
Genetics 107: 295-306).
if
3
phenotype: Longitudinal veins thickened, especially at wing
3 3
base. Anterior crossvein thickened. if /if flies show
reduced levels of PS2 integrin on the surfaces of some
imaginal disc cells (especially in the ventral region), but
levels of this integrin in muscle, salivary glands, and most
other tissues seem to be normal (Brower and Jaffe, 1989).
Adult wings typically show large round wing blisters, but
the penetrance of this phenotype in homo- and hemizygotes
3 k27e
is variable. if /if
flies show an increase in penetrance
(from 15-20% in homozygotes to 60-70% in the
3 k27e
heteroalleles); penetrance is reduced in if /if
flies by
low temperature and crowding (Brower and Jaffe, 1989).
if: inflated
location: 1-55.
references: Brower, Wilcox, Piovant, Smith, and Reger,
1984, Proc. Nat. Acad. Sci. USA 81: 7485-89.
Wilcox, Brown, Piovant, Smith, and White, 1984, EMBO J.
3: 2307-13.
Bogaert, Brown, and Wilcox, 1987, Cell 511: 929-40.
Leptin, Aebersold, and Wilcox, 1987, EMBO J.
6: 1037-43.
Brower and Jaffe, 1989, Nature (London) 342: 285-87
Brown, King, Wilcox, and Kalfatos, 1989, Cell 59: 185-95.
phenotype: Structural gene for the -subunit of position
specific integrin 2 (PS2), a large transmembrane protein
(Bogaert et al., 1987). The -subunit can associate with
either of the two -subunits, PS1 or PS2 (Brower et al.,
1984; Wilcox, Brown, Piovant, Smith, and White, 1984,
EMBO J. 3: 2307-13). Both  and  integrin are expressed
in embryonic and larval tissues. In early development, PS2
is found in the mesoderm, localized to muscle attachments
(Bogaert et al., 1987). Later, PS1 is expressed in the
presumptive dorsal epithelium of the third instar imaginal
wing discs; also, PS2 is found in the ventral epithelium,
both integrins being important for the joining of the dorsal
and ventral surfaces of the wing blade (Brower and Jaffe,
1989). Null mutations cause embryonic lethality (Wilcox,
1
DiAntonio, and Leptin). In the mutant if , the adult wing is
inflated with lymph and smaller than normal; venation is
defective. Wings later become dry and blistered.
alleles:
alleles
if1
if3 
ifk27e
ifN 
origin
discoverer
ref 
spont
Weinstein, 1916
4
spont
Curry, 38b
1, 2
neutrons
Schalet
comments
poorly viable and fertile
resembles if1
1
3
viable and fertile; wing
phenotype resembles if3
if
N
other infornation: Allele induced simultaneously with a f
mutation (Schalet et al., 1983).
If: Irregular facets
location: 2-107.6 [0.6 unit to the right of sp, according to
Ives; inseparable from Kr by recombination in 2589
opportunities.
(Wieschaus, N usslein-Volhard, and
Kluding, 1984, Dev. Biol. 104: 172-86)].
origin: Spontaneous.
discoverer: Casey, 65l16.
references: Ives, 1967, DIS 42: 39.
Renfranz and Benzer, 1989, Dev. Biol. 136: 411-29.
phenotype: In heterozygote, eye area about one-half normal;
narrow and pointed ventrally; facets irregular and often
missing across middle of eyes, sometimes fused or absent
in ventral portion. In homozygote, eyes are narrow slits
with smooth glossy surface. In the eye disk of late third
instar larvae, fairly large number of cell clusters in irregular
arrangement, especially in ventral half of disk (Renfranz
and Benzer, 1989). Viability and fertility good. RK1.
cytology: Placed in 60F3 on the basis of the concordant
API
reversion of If and induction of Kr
associated with a
molecularly, but not cytologically, discernable deletion of
+

1 = Brower and Jaffe, 1989, Nature (London) 342: 285-87; 2 = Curry,
1939, DIS 12: 45; 3 = Schalet, Leigh, and Paradi, 1983, Proc. Int.
Congr. Rad. Res. 7th, pp. c4-12; 4 = Weinstein, 1918, Genetics 3: 157.

Kr . (Preiss, Rosenberg, Kienlin, Seifert, and J aekle,
1985, Nature 313: 27-32).
Ifm: Indirect flight muscle (J.C. Hall)
A
collection
of
ethyl-methanesulfonate-induced
autosomal dominant flight-defective mutants characterized
by Mogami and Hotta (1981, Mol. Gen. Genet.
183: 409-17). Heterozygotes frequently hold wings up.
Fine structure examination of myofibrils reveals
abnormalities in every case, and in some cases particular
proteins missing from three-dimensional gels of
homozygotes. Specific features detailed in the following
entries.
Ifm(2)3: see Mhc
Ifm(2)11
location: 2-56 (just to right of pr).
phenotype: 10% of homozygotes hold wings erect.
Myofibrils have thin or ruptured A bands; may appear faint.
other information: Fails to complement Ifm(2)3 even though
it maps to a separate second-chromosome region.
Ifm(3)1: see Act88F
Ifm(3)2: see Act88F
Ifm(3)3: see Tm2
Ifm(3)4: see Act88F
Ifm(3)5, Ifm(3)6
location: 3-55 (between red and ss).
phenotype: Homozygotes for Ifm(3)5 and Ifm(3)6 display
characteristic departures from wild-type protein patterns in
two-dimensional gels (Mogami and Hotta, 1981). Ifm(3)5
homozygotes lack myofibrils; Ifm(3)6 homozygotes have
opaque strings of myofibrils. Both mutants are flightless as
heterozygotes. The myofibrils of Ifm(3)6 heterozygotes are
frayed.
other
information: Ifm(3)5
and
Ifm(3)6
are
recombinationally inseparable.
Ifm(3)7: see Act88F
*im: interrupted margin
location: 1-3.1.
origin: Induced
by
2-chloroethyl
methanesulfonate
(CB. 1506).
discoverer: Fahmy, 1956.
references: 1959, DIS 33: 86-87.
phenotype: Wing margin nicked to various degrees with
costal vein frequently interrupted. Extra wing venation
often present and occasionally anastomoses, giving a
plexus, particularly at the wing apex. Eyes smaller and
sometimes slightly rough. Bristles thin. Males small, late
eclosing; viability reduced. Female sterile. RK3.
Imp-E: Inducible membrane-bound polysomes-Early
origin: From imaginal disc cultures treated with
20-hydroxyecdysone.
references: Natzle, Hammonds, and Fristrom, 1986, J. Biol.
Chem. 261: 5575-83.
Natzle, Fristrom, and Fristrom, 1988, Dev. Biol.
129: 428-38.
phenotype: Name given to three genes encoding transcripts
associated with membrane-bound polysomes in imaginal
discs
and
expressed
only
in
response
to
20-hydroxyecdysone (20 HOE). Expression studied both in
vitro and in vivo. Imp-E denotes three "early" genes
involved in elongation of appendage-forming regions of the
imaginal discs by means of epithelial-cell rearrangements
(Natzle et al., 1988).
cytology: Three Imp-E genes have been isolated; their
cytological location as determined by in situ hybridization
is shown in the following table.
gene
location
Imp-E1  3-{26}
Imp-E2
3-{6}
Imp-E3
3-{48}
cytology
66C
63E
84E

Present in single copy.
molecular biology: Genes cloned by use of a hybridization
screen for ecdysone inducible expression in imaginal discs
(Natzle et al., 1986). Imp-E1 probe detects a 7.5 kb
transcript in cultured imaginal discs treated with 20-HOE as
well as in imaginal discs from third instar larvae and white
pupae, where transcript occurs in leg, wing, haltere, and
genital discs, but not in the ommatidial region of the
eye-antennal discs (Natzle et al., 1988). The transcript
accumulates rapidly after 20-HOE treatment, but no
transcript is found without ecdysone. In vivo, the 7.5 kb
transcript can be detected, not only in larvae in the imaginal
discs, but also (after pupariation) in glial cells around the
brain. The gene product is believed to be involved in cell
rearrangements in the epithelium of imaginal discs and in
the glial layers (Natzle et al., 1988).
Imp-L: Imp-Late
origin: From imaginal disc cultures treated with
20-hydroxyecdysone.
references: Natzle, Hammonds, and Fristrom, 1986, J. Biol.
Chem. 261: 5575-83.
Osterbur, Fristrom, Natzle, Tojo, and Fristrom, 1988, Dev.
Biol. 129: 439-44.
phenotype: Imp-L encoding transcripts associated with
membrane-bound polysomes in imaginal discs and
expressed only in response to 20-hydroxyecdysone (20
HOE). Expression studied both in vitro and in vivo. Imp-L
denotes three "late" genes involved in the eversion to the
exterior of the elongated regions of discs by means of local
changes in cell shape (Osterbur et al., 1988).
cytology: Three Imp-L genes have been isolated; their
cytological location as determined by in situ hybridization
is shown in the following table.
gene
location
cytology
Imp-L1
3-{40}
70A
Imp-L2  3-{12}
Imp-L3
3-{21}
64B
65B

Present in single copy.
molecular biology: Genes cloned by use of a hybridization
screen for ecdysone-inducible expression is found in
imaginal discs (Natzle et al., 1986). Imp-L3 probe detects a
3.0 transcript in cultured imaginal discs treated with
20-HOE as well as in third instar larvae and pupae
(maximum transcript accumulation occurring just after
pupation). In vivo, the 3.0 transcript can be detected in cells
of the peripodial epithelium (precursors of head and thorax
epithelium) and later in the imaginal histoblasts (precursors
of the adult abdominal epithelium) (Osterbur et al., 1988).
The gene product may be involved in the flattening of the
epithelial cells in preparation for fusion into a contiguous
sheet.
in: inturned
location: 3-46.75 (Araj arvi and Hannah-Alava, 1969, DIS
44: 73-4).
origin: Spontaneous.
discoverer: Bridges, 26k20.
references: Gubb
and
Garc<OVERSTRIKE<'i>OVERSTRIKE>a-Bellido,
1982, J. Embryol. Exp. Morphol. 68: 37-57.
phenotype: Hairs and bristles on thorax and abdominal
tergites, directed irregularly toward midline; trichomes and
chaetae on mesonotum coordinately misdirected (Toney
and Thompson, 1980, Experientia 36: 344-45). Marginal
hairs of wing stand out from wing margin; trichomes on
wing blade no longer directed in parallel with longitudinal
veins; frequently divergent therefrom.
50-60% of
trichome-bearing cells express duplicated or rarely
triplicated trichomes. Wings slightly spread and tend to be
long and narrow. Somatic clones of homozygous cells in
wing
described
by
Gubb
and
Garc<OVERSTRIKE<'i>OVERSTRIKE>a-Bellido.
Incomplete extra leg joints tend to form as mirror-image
duplications proximal to the normal joints on tarsal
segments three and four (Held, Duarte, and Derakhshanian,
1986, Wilhelm Roux’s Arch. Dev. Biol. 195: 145-57).
RK1.
alleles:
allele
origin
discoverer
ref 
cytology
in1
in60
spont
Bridges, 26b20
3, 4
+
1
T(2;3)
1, 5
Dp(1;3)
in61j2
inSS306
X ray
S. Smith
2
inwvco
X ray
Clausen
3, 4
T(1;3)wvco
1 = Araj arvi and Hannah-Alava, 1969, DIS 44: 73; 2 = Ashburner,
Faithfull, Littlewood, Richards, Smith, Velissariou, and Woodruff,
1980, DIS 55: 193-95; 3 = CP552; 4 = CP627; 5 = Hannah-Alava,
1971, Mol. Gen. Genet. 113: 191-203.
61j2
cytology: Placed in 77C on the basis of Dp(1;3)in
=
Dp(1;3)20;77C, an insertion of the nucleolus organizer into
3L (Hannah-Alava, 1971, Mol. Gen. Genet. 113: 191-203).
In-ho: see ho40
inaA: inactivation-no-afterpotential-A (J. Hall)
location: 2-44 (between Sp and Bl).
origin: Induced by ethyl methanesulfonate.
inaB (J.C. Hall)
location: 2-{14} (between S and Sp).
origin: Induced by ethyl methanesulfonate.
references: Pak, 1979, Neurogenetics: Genetic Approaches
to the Nervous System (Breakefield, ed.). Elsevier, New
York, pp. 67-99.
phenotype: Same basic phenotype as inaA; also, inaB lacks
on and off transient spikes of electroretinogram (ERG).
1
2
alleles: Two mutant alleles inaB and inaB , formerly P222
and P223.
cytology: Located in 25CD-28B. Normal allele carried by
P D
Y 2 element of T(1;Y)H52 = T(1;Y)28B, but not by that of
T(1;Y)D6 = T(1;Y)25C-D (Pye).
inaC (J.C. Hall)
location: 2-82 (distal to L).
origin: Induced by ethyl methanesulfonate.
references: Pak, 1979, Neurogenetics: Genetic Approaches
to the Nervous System (Breakefield, ed.). Elsevier, New
York, pp. 67-99.
phenotype: Same basic phenotype as inaA; also, inaC lacks
off transient of ERG, and (in such physiological recordings)
there is a slow return to baseline potential at stimulus
offset.
1
3
alleles: Eight; inaC - inaC isolated by Pak as P207, P209,
4
8
and P234; inaC - inaC isolated in Merriam’s laboratory
as US2167, US3741, US3841, US4173, and US4186.
inaD (J.C. Hall)

In-f: see E(f)
references: Pak, 1979, Neurogenetics: Genetic Approaches
to the Nervous System (Breakefield, ed.). Elsevier, New
York, pp. 67-99.
phenotype: Mutant eyes lack the prolonged depolarizing
afterpotential (PDA) that is induced in wild-type R1-6
photoreceptors by a bright or prolonged blue light stimulus,
which photoconverts a large fraction of rhodopsin in these
photoreceptors to metarhodopsin; inaA-induced phenotype
differs from that observed in nina mutants because the R1-6
photoreceptors of ina mutants are inactivated after the blue
stimulus, i.e., are insensitive to subsequent blue light
stimuli; an orange light stimulus, which cancels the PDA of
wild type by photoconverting metarhodopsin back to
rhodopsin, restores the R1-6 cell sensitivity of ina mutants.
alleles: One allele isolated as P226.
location: 2-101.
origin: Induced by ethyl methanesulfonate.
references: Pak, 1979, Neurogenetics: Genetic Approaches
to the Nervous System (Breakefield, ed.). Elsevier, New
York, pp. 67-99.
phenotype: Semi-dominant mutant of visual physiology,
such that the phenotype (re PDA) of heterozygote similar to
that produced by other ina homozygotes; inaD
homozygotes exhibit ERG response that decays to baseline
during bright light stimulus, and off transient is absent.
alleles: One mutant allele, isolated as P215.
cytology: Located between 58F1 and 60F1, based on
+
+ +
coverage by bw duplication in bw Yy .
inaE (J.C. Hall)
location: 1 (unlocalized).
origin: Induced by ethyl methanesulfonate.
references: Pak, 1979, Neurogenetics: Genetic Approaches
to the Nervous System (Breakefield, ed.). Elsevier, New
York, pp. 67-99.
phenotype: Same basic eye-physiology phenotype as in
1
inaA, inaB, and inaC; one allele (at least, i.e. inaE ) causes
age-dependent photoreceptor degeneration.
1
2
alleles: Two mutant alleles; inaE and inaE isolated as N125
and P19.
inactive: see iav
*inb: incised balloon
location: 2-55.
origin: Spontaneous.
discoverer: Neel, 41d9.
references: 1942, DIS 16: 50.
phenotype: Wings held at 45° angle to body. Wing margins
incised, varying from slight nicks to extreme reduction to
small fluid-filled sacs. RK2.
cytology: Salivary chromosomes normal.
*Ind: Indented
location: 2-63.
origin: Spontaneous.
discoverer: Cole, 40e.
references: Whittinghill and Parker, 1945, Genetics
30: 27-28.
Whittinghill, 1947, DIS 21: 72.
phenotype: Eye usually kidney shaped with indentation
anteriorly; shape sometimes normal but facets irregular.
Often indented posteriorly as well as anteriorly, sometimes
dividing eye into two spots or with only upper lobe
persisting. Rarely eyeless. More extreme at 28° than at
25°. RK2.
indented thorax: see int
Indirect flight muscle: see Ifm
Inducible membrane-bound polysomes:
see Imp-E and Imp-L
inflated: see if
infrabar: see Bi
infrabar Bar: see BBi
Inosine dehydrogenase: see bur
Inr: Insulin receptor
location: 3-{72}.
references: Petruzzelli, Herrera, Garcia, and Rosen, 1985a,
Cancer Cells: 115-21.
1985b, J. Biol. Chem. 260: 16072-75.
Nishida, Hata, Nishizuka, Rutter, and Ebina, 1986,
Biochem. Biophys. Res. Commun. 141: 474-81.
Petruzzelli, Herrera, Arenas-Garcia, Fernandez, Birbaum,
and Rosen, 1986, Proc. Nat. Acad. Sci. USA 83: 4710-14.
Fernandez-Almonacid and Rosen, 1987, Mol. Cell Biol.
7: 2718-27.
phenotype: Encodes
the
insulin-binding
()
and
insulin-dependent protein tyrosine kinase () subunits of
the insulin receptor of Drosophila melanogaster. In
Drosophila cell lines the insulin receptor contains
insulin-binding  subunits of 110 or 120 kd, a 95-kd 
subunit that is phosphorylated on tyrosine in response to
insulin, and a 170-kd protein that may be an incompletely
processed receptor. All of the components are processed
from a proreceptor, joined by disulfide bonds, and exposed
on the cell surface (Petruzzelli et al., 1985a, 1985b, 1986;
Fernandez-Almonacid and Rosen, 1987). Subunits in man
and in Drosophila are similar both in molecular structure
and in insulin-binding and protein tyrosine kinase activities;
the latter activity is detected only during certain embryonic
periods in Drosophila.
cytology: Located in 93E by in situ hybridization of cloned
DNA (Rosen and Young; confirmed by Chovnick); single
copy gene.
molecular biology: Inr has been cloned using human -and
-subunit-specific probes (Nishida et al., 1986; Petruzzelli
et al., 1986); nucleotide and deduced amino acid sequences
of the kinase domain of the  subunits have been obtained.
Fourteen clones hybridized to the human  subunit; two
clones hybridized to the human  subunit. A cDNA probe
detects mRNA’s of 8.6 and 11 kb. The 86-kb mRNA is
relatively frequent in oocytes and early embryos whereas
the 11-kb message is more prevalent in later embryos, in
the developing nervous system and in imaginal discs
(Garofalo and Rosen, 1988, Mol. Cell Biol. 8: 1638-47).
int: indented thorax
location: 1-43.5.
origin: Induced by ethyl methanesulfonate.
discoverer: Ghysen.
references: Deak, 1977, J. Embryol. Exp.
40: 35-63.
Morphol.
Deak, Bellamy, Bienz, Dubuis, Fenner, Gollin, R ahmi,
Ramp, Reinhardt, and Cotton, 1982, J. Embryol. Exp.
Morphol. 69: 61-81 (fig.).
Homyk and Emerson, 1988, Genetics 119: 105-21.
phenotype: 80-85% of int flies hold wings ventrolaterally,
10% hold them vertically and the remainder maintain
normal wing position. In many flies mesonotum indented to
variable degree and at various positions; 85% in flies raised
at 29° and 45% when raised at 18°. More extreme
expression in y flies; partially dominant in y genotypes.
Fate mapping indicates focus in presumptive thoracic
musculature.
Indirect flight muscle structure badly
deranged, Z-bands disappear as muscles degenerate; also
lose a 54k protein. int/int adults flightless and unable to
jump; int/+ adults normal.
1
2
3
4
alleles: int , int , int and int mentioned in Deak et al..
other information: Claimed to be allelic to up (1-43.5) by
Deak et al., 1982 but earlier mapping data of Deak not
reconciled; therefore tentatively considered to be a separate
locus.
 Integrin: see if
 Integrin: see mys
intensifier: see e( )
Intensifier: see E( )

interrupted margin: see im
W
12
Interruptus: see ci
intersex: see ix
intersex on chromosome 3: see dsx60l
cytology: Located in 20A (Lefevre and Watkins, 1986).
intersex-62c: see dsx
inv: invected
intro: introvert
location: 1-66.
references: Schalet and Lefevre, 1973, Chromosoma
44: 183-202.
Schalet and Lefevre, 1976, The Genetics and Biology of
Drosophila (Ashburner and Novitski, eds.). Academic
Press, London, New York, San Francisco, Vol. 1b, pp.
847-902.
Lefevre and Watkins, 1986, Genetics 113: 869-95.
Schalet, 1986, Mutat. Res. 163: 115-44.
Perrimon, Smouse, and Miklos, 1989, Genetics
121: 313-31.
Schlosser, Boschert, and Fischbach, unpublished data.
phenotype: Many mutants exhibit a pupal lethal phase,
although some are larval lethals. [The name "introvert" is
derived from abnormality of some hemizygous pupae in
which the head remains inverted within the thorax
(Schlosser et al.)]. Pupal-phase mutants do not contract at
the beginning of pupation, remaining slender like larvae.
Eye development very rudimentary. Germline clone
analysis shows variable lethal phenotypes, including
collapsed eggs (Perrimon et al.).
alleles:
allele
intro1
intro2
intro3
intro4
intro5
intro6
intro7
intro8
intro9
intro10
intro11
12
intro
intro13
intro14
intro15 
intro16
13
Most flies exhibit a pupal lethal phase like intro and intro . However,
those males and females that eclose and mate appear normal and are
12
13
fertile (Schalet, 1986). Viability of heterozygotes with intro or intro
is low (5% or less).
origin
discoverer
synonym
ref 
comments
EMS
Lifschytz
l(1)M28
4
on y+Ymal+
EMS
Lifschytz
l(1)Q2
3
EMS
Lifschytz
l(1)Q56
2, 3, 5, 6
EMS
Lifschytz
l(1)R-9-3
3
EMS
Lifschytz
l(1)R-9-13
3
X ray Lefevre
l(1)A125
T(1;3)18F-19A;20;83C
1
X ray Lefevre
T(1;2)20A-B;27-28
l(1)GE214
1
X ray
Lefevre
l(1)HF381
1
EMS
Lefevre
l(1)DC789
2
EMS
Lefevre
l(1)VA42
2
EMS
Lefevre
l(1)VE793
2
spont
Schalet
l(1)11-55
7
spont
Schalet
l(1)19-98
7
mei-9
Schalet
l(1)18-1
mei-9
Schalet
l(1)M1-5
EMS
Lifschytz
l(1)YT1
4
on mal+Y

location: 2-{62} (located immediately to the left of en).
synonym: engrailed-related.
references: Poole, Kauvar, Drees, and Kornberg, 1985, Cell
40: 37-43.
Coleman, Poole, Wier, Soeller, and Kornberg, 1987, Genes
Dev. 1: 19-28.
Drees, Ale, Soeller, Coleman, Poole, and Kornberg, 1987,
EMBO J. 6: 2803-09.
phenotype: Although a developmental role for inv is
indicated by hybridization, experiments with embryonic
and larval cells using cDNA probes, the function in
development of the protein encoded by inv is not known
(Coleman et al., 1987). No mutant alleles were reported.
cytology: Located in 48A.
molecular biology: DNA spanning the en locus was cloned
by DNA walking using a collection of en mutants of known
cytology (Poole et al., 1985). Two clones obtained from
this region indicated the presence of another gene located
17 kb proximal to en. Unlike en, this gene (inv) is
transcribed from left to right (Poole et al., 1985; Coleman
et al., 1987). Nucleotide sequences and presumed amino
acid sequences were obtained. inv shows striking sequence
identity to en (52 out of 60 amino acids identical) at the
carboxy-terminal end in a 117-amino-acid region
containing homeobox sequences; however, no sequence
similarities were observed elsewhere in the presumed
protein-coding region, which is similar in size in both genes
(1740 bp in inv and 1656 bp in en). inv has four exons of
1588, 6, 161, and 694 bp and three introns; the first intron,
the second exon, and the second intron span about 26 kb,
the third intron (417 bp) splits the homeobox. Genomic
DNA probes from inv hybridized to transcripts of 3.4, 2.7,
and 1.2 kb (Poole et al., 1985; Drees et al., 1987); the
2.7-kb transcript is believed to represent the mature
invected mRNA (Coleman et al., 1987). This mRNA is
thought to encode a 576-amino acid protein of about 60 kd.
cDNA probes specific to inv and en were used for in situ
hybridization to sections from embryos, larvae, and
imaginal discs. Both genes were expressed in the posterior
developmental compartment of embryonic and larval cells,
as well as in the hindgut, clypolabrum and neural ganglia,
but inv expression appeared at a later period than en
expression (Coleman et al., 1987).
inturned: see in
invected: see inv
1 = Lefevre, 1981, Genetics 99: 461-80; 2 = Lefevre and Watkins,
1986, Genetics 113: 869-95; 3 = Lifschytz and Falk, 1969, Mutat. Res.
8: 147-55; 4 = Lifschytz and Yakabovitz, 1978, Mol. Gen. Genet.
161: 275-84; 5 = Schalet, 1986, Mutat. Res. 163: 115-44; 6 = Schalet
and Lefevre, 1973, Chromosoma 44: 183-202; 7 = Schalet and Lefevre,
1976, The Genetics and Biology of Drosophila (Ashburner and
Novitski, eds.). Academic Press, London, New York, San Francisco,
Vol. 1b, pp. 847-902.
irreC: irregular chiasm-C (J.C. Hall)
1
location: 1-1.7 (from cytology, association with rst; irreC
does map between y and cv).
references: Boschert, Ramos, Tix, Technau, and Fischbach,
1990, J. Neurogenet. 6: 153-71.
phenotype: In optic ganglia, fiber tracts from the medulla to
the lobula plate penetrate lobula neuropile instead of
projecting through second optic chiasm; occasionally,
ectopic bundles of axonal fibers penetrate lobula-plate
neuropile; in most severely deformed individuals, lobula
and lobula plate are partly fused. In first optic chiasm,
fibers from lamina are misrouted, taking detour around
posterior medulla neuropile, penetrating the latter at
variable positions on its inner (posterior) face from which
positions the fiber tracts turn around and form
normal-appearing terminals in retinotopic locations.
Gynandromorph analysis showed that eye genotype does
not induce optic lobe phenotypes. It also appears as if
first- (or second-) chiasm defect does not induce that in the
second (or first); among several mutant individuals
analyzed (cf. variable expressivity under alleles), there is no
correlation between the anatomical abnormalities in these
two locations (though there is high correlation between
defective first or second chiasm in left and right sides of
head). Optic lobe pioneer axons [larval neurons, which
persist into adulthood and can be seen following path of
first optic chiasm, and may guide newly growing fibers
during formation of imaginal visual system (Tix, Minden,
and Technau, 1989, Development 105: 739-46)] are
displaced in irreC pupae, with their axons having followed
ectopic pathways.
1
UB883
alleles: irreC (P-element induced as irreC
) shows 94%
penetrance for optic-lobe defects; good viability and
fertility; expressivity highly variable (e.g., anatomical
abnormalities can appear in only first but not second
chiasm, or vice versa, or in only left or right side of the
2
IR34
head). IrreC (X ray induced as irreC
) shows high
penetrance for optic-lobe abnormalities, but variable
expressivity; females homozygous for this inversion (see
below) do not lay eggs and have rudimentary egg chambers
(likely not due to lesion in region 3C, owing to fertility of
synthetic deletion described under cytology).
1
cytology: Located in 3C4-5. irreC has a P element inserted
2
in 3C (also in 2EF and 4D); irreC is associated with
In(1)2A;3C3-6, with anatomical defects inseparable from
the inversion. The following deletions uncovered irreC
mutation(s): Df(1)JC19 = Df(1)2F6;3C5, Df(1)N8 =
Df(1)3C2-3;3E3-4, Df(1)w258-42 = Df(1)3A4-6;3C5-6,
and Df(1)N71h
= Df(1)3C4;3D3-4; the nearest
complementing deletions tested were Df(1)258-45 =
Df(1)3B2-3;3C2-3 and Df(1)N69h9 = Df(1)3C6;3D1.
Females heterozygous for Df(1)w258-42/Df(1)N8 are
irreC-like in their optic lobe anatomy (as well having white
and roughest eyes, and seem no worse so than mutant
homozygotes or hemizygotes; such females are also fertile.
other information: Associated with the closely linked rst
6
locus. Whereas two mutant rst alleles (including rst ) lead
to no apparent abnormalities in optic chiasms (cf.
Meyerowitz and Kankel, 1978, Dev. Biol. 62: 112-42), and
1
irreC causes no eye roughening, this mutation over
2
Df(1)rst vt leads to rough eyes; some irreC flies show
6
weak eye roughening, and that allele over rst exhibits
rough eyes but normal optic lobes.
Irregular facets: see If
It: see ciW
ix: intersex
location: 2-60.5.
origin: Spontaneous.
discoverer: L. V. Morgan, 1943.
references: Morgan, Redfield, and Morgan, 1943, Year Book
- Carnegie Inst. Washington 42: 171-74.
Kroeger, 1959, Arch. Entwicklungsmech. Organ.
151: 301-22 (fig.).
Baker and Belote, 1983, Annu. Rev. Genet. 17.
McRobert and Tompkins, 1985, Genetics 111: 89-96.
phenotype: Females changed into sterile intersexes with a set
of reduced male and a set of irregular female external
genitalia. Gonads also mixed. They have no sex combs;
pigmentaion of abdomen intermediate between male and
female. A large mass of chitinized tissue protrudes from
vaginal opening. Homozygous males look normal but
behave like intersexes (McRobert and Tompkins, 1985).
They court young males as much as normal males do, and
occasionally court females; however, they are attractive to
normal mature males. Heterozygous ix/+ males court
females and young males, but seldom court mature males.
The ix locus acts with the dsx female function to allow
somatic differentiation in females (Nagoshi, McKeown,
Burtis, Belote, and Baker, 1988, Cell 53: 229-36).
2
ix
origin: Ultraviolet induced.
discoverer: Meyer, 50k.
synonym: tom: tomboy.
references: Meyer and Edmondson, 1951, DIS 25: 73.
Meyer, 1958, DIS 32: 83.
2
phenotype: Females homozygous for ix have male-like
pigmentation of posterior tergites, rudimentary ovaries, and
are sterile. Expression extreme and viability reduced at
27°; at 17°, expression less extreme and viability greater.
Homozygous males appear normal but have nonmotile
sperm. RK2.
other information: The possibility that the male sterility is at
another locus has not been excluded.
3
ix
origin: Induced by ethyl methanesulfonate.
discoverer: Duncan.
D100.36
synonym: ix
.
references: Nagoshi, McKeown, Burtis, Belote, and Baker,
1988, Cell 53: 229-36.
Ix: see BX-C
ix62C: see dsx
ix-3: see dsx60l