i:  see E(B)

 I:  see E(B)

 I-f:  see E(f)

 iab:  see BXC

 iav:  inactive (J.C. Hall)
location:  1-18.8 (iav1), 20.7 (hypoB1).
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.
phenotype:  iav1 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, but settles into inactivity soon afterward. iav2 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). Gynandromorph analysis of iav2 adult behavioral impairments suggests primary focus could be neural (Homyk, 1977). Open-field activity tests of iav1 and iav2 (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 activity increase (in tests of iav2) in parallel between days 1 and 2 of adulthood (reaching a much lower than normal plateau).  In tests of homozygous iav1 and iav2 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.
alleles:  iav1, spontaneous (Kaplan, 1977), iav2, iav3, induced by ethyl methanesulfonate [originally hypoB1-3 (Homyk and Sheppard, 1977)].
other information:  Allelism of iav1 to hypoB1 shown by O’Dell and Burnet (1986) in open field tests of heterozygotes; they also note that both mutations are recessive.

 Ic D:  see bwVD

 Idh:  Isocitrate dehydrogenase 
location:  3-25.4 [based on Ohnishi and Voelkers mapping of IdhF vs IdhS 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 (1983, Biochem. Genet. 21:  725-33) mapping of IdhnGB1 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 of a hybrid dimer in IdhF/IdhS 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 a	residual	heterodimer	
			activity	formation	
					
IdhF	Idh6	3, 4			
IdhnGB1		2, 6, 7	0	+	
IdhnGB2	IdhGB2	1, 2, 6, 7	5% b	-	
IdhnNC1		2, 6, 7	0	+	
IdhS	Idh4	3, 4			
IdhSS	Idh2	5			

a

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.
b

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:  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 a-subunit of position specific integrin 2 (PS2), a large transmembrane protein (Bogaert et al., 1987). The b-subunit can associate with either of the two a-subunits, PS1 or PS2 (Brower et al., 1984; Wilcox, Brown, Piovant, Smith, and White, 1984, EMBO J. 3:  2307-13). Both a and b 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, DiAntonio, and Leptin). In the mutant if1, the adult wing is inflated with lymph and smaller than normal; venation is defective. Wings later become dry and blistered.
alleles:  

alleles	origin	discoverer	ref a	comments	
					
if1	spont	Weinstein, 1916	4	poorly viable and fertile 	
if3 b	spont	Curry, 38b	1, 2	resembles if1 	
ifk27e			1 		
ifN b	neutrons	Schalet	3	viable and fertile; wing	
				phenotype resembles if3 	

a

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.
b

Further descriptions below.

cytology:  Located in 15A1-5 by in situ hybridization of cloned DNA (Bogaert et al., 1987).
molecular biology:  The gene encoding the PS2 a-subunit has been cloned, genomic and cDNA sequences obtained (Bogaert et al., 1987). The predicted N terminus of the PS2 a-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 a-subunits of the vertebrate fibronectin receptor family (Bogaert et al., 1987; Leptin et al., 1987). The C-terminal region of the Drosophila a-subunit that shows no identity to the vertebrate a-subunit is characterized by the presence of multiple serine repeats.

 if3 
phenotype:  Longitudinal veins thickened, especially at wing base. Anterior crossvein thickened. if3/if3 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 is variable. if3/ifk27e flies show an increase in penetrance (from 15-20% in homozygotes to 60-70% in the heteroalleles); penetrance is reduced in if3/ifk27e flies by low temperature and crowding (Brower and Jaffe, 1989).

 ifN 
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 reversion of If and induction of KrAPI associated with a molecularly, but not cytologically, discernable deletion of 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	cytology	
			
Imp-E1 a	3-{26}	66C 	
Imp-E2	3-{6}	63E 	
Imp-E3	3-{48}	84E 	

a

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 a	3-{12}	64B 	
Imp-L3	3-{21}	65B 	

a

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 a	cytology	
					
in1	spont	Bridges, 26b20	3, 4	+	
in60			1	T(2;3)	
in61j2			1, 5	Dp(1;3)	
inSS306	X ray	S. Smith	2		
inwvco	X ray	Clausen	3, 4	T(1;3)wvco	

a

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.

cytology:  Placed in 77C on the basis of Dp(1;3)in61j2 = Dp(1;3)20;77C, an insertion of the nucleolus organizer into 3L (Hannah-Alava, 1971, Mol. Gen. Genet. 113:  191-203).

 In-f:  see E(f)

 In-ho:  see ho40

 inaA:  inactivation-no-afterpotential-A (J. Hall)
location:  2-44 (between Sp and Bl).
origin:  Induced by ethyl methanesulfonate.
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.

 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).
alleles:  Two mutant alleles inaB1 and inaB2, formerly P222 and P223.
cytology:  Located in 25CD-28B. Normal allele carried by YP2D 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.
alleles:  Eight; inaC1 - inaC3 isolated by Pak as P207, P209, and P234; inaC4 - inaC8 isolated in Merriam’s laboratory as US2167, US3741, US3841, US4173, and US4186.

 inaD (J.C. Hall)
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 inaA, inaB, and inaC; one allele (at least, i.e. inaE1) causes age-dependent photoreceptor degeneration.
alleles:  Two mutant alleles; inaE1 and inaE2 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 (a) and insulin-dependent protein tyrosine kinase (b) subunits of the insulin receptor of Drosophila melanogaster. In Drosophila cell lines the insulin receptor contains insulin-binding a subunits of 110 or 120 kd, a 95-kd b 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 a-and b-subunit-specific probes (Nishida et al., 1986; Petruzzelli et al., 1986); nucleotide and deduced amino acid sequences of the kinase domain of the b subunits have been obtained. Fourteen clones hybridized to the human a subunit; two clones hybridized to the human b 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. Morphol. 40:  35-63.
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.
alleles:  int1, int2, int3 and int4 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.

 a Integrin:  see if

 b Integrin:  see mys

 intensifier:  see e( )

 Intensifier:  see E( )

 interrupted margin:  see im

 Interruptus:  see ciW

 intersex:  see ix

 intersex on chromosome 3:  see dsx60l

 intersex-62c:  see dsx

 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	origin	discoverer	synonym	ref a	comments	
						
intro1	EMS	Lifschytz	l(1)M28	4	on y+Ymal+	
intro2	EMS	Lifschytz	l(1)Q2	3		
intro3	EMS	Lifschytz	l(1)Q56	2, 3, 5, 6		
intro4	EMS	Lifschytz	l(1)R-9-3	3		
intro5	EMS	Lifschytz	l(1)R-9-13	3		
intro6	X ray	Lefevre	l(1)A125	1	T(1;3)18F-19A;20;83C	
intro7	X ray	Lefevre	l(1)GE214	1	T(1;2)20A-B;27-28	
intro8	X ray	Lefevre	l(1)HF381	1		
intro9	EMS	Lefevre	l(1)DC789	2		
intro10	EMS	Lefevre	l(1)VA42	2		
intro11	EMS	Lefevre	l(1)VE793	2		
intro12	spont	Schalet	l(1)11-55	7		
intro13	spont	Schalet	l(1)19-98	7		
intro14	mei-9	Schalet	l(1)18-1 			
intro15 b	mei-9	Schalet	l(1)M1-5 			
intro16	EMS 	Lifschytz	l(1)YT1	4	on mal+Y 	

a

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.
b

Most flies exhibit a pupal lethal phase like intro12 and intro13. However, those males and females that eclose and mate appear normal and are fertile (Schalet, 1986). Viability of heterozygotes with intro12 or intro13 is low (5% or less).

cytology:  Located in 20A (Lefevre and Watkins, 1986).

 inv:  invected 
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

 irreC:  irregular chiasm-C (J.C. Hall)
location:  1-1.7 (from cytology, association with rst; irreC1 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.
alleles:  irreC1 (P-element induced as irreCUB883) 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 head).  IrreC2 (X ray induced as irreCIR34) 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).
cytology:  Located in 3C4-5.  irreC1 has a P element inserted in 3C (also in 2EF and 4D); irreC2 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 locus. Whereas two mutant rst alleles (including rst6) lead to no apparent abnormalities in optic chiasms (cf. Meyerowitz and Kankel, 1978, Dev. Biol. 62:  112-42), and irreC1 causes no eye roughening, this mutation over Df(1)rst vt leads to rough eyes; some irreC2 flies show weak eye roughening, and that allele over rst6 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).

 ix2 
origin:  Ultraviolet induced.
discoverer:  Meyer, 50k.
synonym:  tom:  tomboy.
references:  Meyer and Edmondson, 1951, DIS 25:  73.
Meyer, 1958, DIS 32:  83.
phenotype:  Females homozygous for ix2 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.

 ix3 
origin:  Induced by ethyl methanesulfonate.
discoverer:  Duncan.
synonym:  ixD100.36.
references:  Nagoshi, McKeown, Burtis, Belote, and Baker, 1988, Cell 53:  229-36.

 Ix:  see BX-C

 ix62C:  see dsx

 ix-3:  see dsx60l