Ax: Abruptex (W.J. Welshons)
From Mohr, 1932, Proc. Intern. Congr. Genet., 6th, Vol. 1: 190-212.
Homozygous females and males show shortened L5 vein,
usually also L4, L2, and sometimes L3. Wings shortened,
arched, and thin. Costal bristles clumped and frayed; costal
veins thickened. Thorax shows midfurrow with rearranged hair
directions; hairs on thorax and head fewer, with clear patches
and streaks. Male genitalia often rotated. Ax/+ females show
short L5 in half of the flies and sparse hair pattern on
thorax. Lower temperature (19) markedly decreases expression,
and higher temperature enhances it. Some Ax alleles enhance N
expression in Ax/N heterozygotes, but others suppress the dominant N phenotype. For example, Ax/N8 approaches wild type in
all characteristics. No wing-vein interruption in Ax/+ at 18
and 26, and enhancement by H occurs so that Ax/Y;H/+ and
Ax/Ax;H/+ are nearly lethal at 26 (House, 1959, Anat. Record
134: 581-82). Ax/Ax;ciD/+ and Ax/Y;ciD/+ are lethal or
nearly so at 26. At 22, males survive and show enhanced
wing-vein interruption and more missing bristles. At 26,
wing-vein interruption approaches 100% in Ax/+;ciD/+ (House
and Lutes, 1975, Genetics 80: s42-43).
Wing nicking is suppressed in Ax/N55e11 at 25, and Ax venation is weakly expressed; Ax/Ax;Dp(1;2)51b/+ shows weak Ax
venation (Portin, 1975, Genetics 81: 121-33). Nearly lethal
when reared at 29; temperature-sensitive period early pupa
(Portin and Sir'n, 1976, Hereditas 84: 109-16). In heterozygotes of Ax with the recessives at Notch at 18 and 25, there
is neither expression of the recessive nor Ax-type venation.
At 29, only Ax/fano shows some weak expression of the recessive, and all heterozygotes except Ax/nd2 show some Ax venation (Portin, 1977, Hereditas 87: 77-84). Ax interacts with
alleles Ax9, Ax59b, Ax71d, Ax16, and AxE2 (see appropriate
entry). RK2 in males.
Temperature-sensitive lethal; male viable at 25 but
nearly lethal at 29. Ax1/AxE2 semilethal at 25 and lethal at
29. Temperature-sensitive period for lethality of Ax1 at
beginning of pupal stage; of Ax1/AxE2 at end of third instar
and into early pupal stage.
Viable in both sexes but poorly fertile or sterile.
Bristle loss and vein interruptions are more extreme at 29.
Heterozygotes of Ax9 with Ax1 and AxE1 are viable, but Ax9 is
inviable with Ax71d, Ax16, and AxE2 (negative complementation). The lethality associated with negative complementation
is suppressed by 23 lethal Notch alleles as well as by alleles
of Dl and mam (Xu, Rebay, Fleming, Scottgale, and Artavanis-Tsakonas). When heterozygous with N mutants, phenotypes of Ax
and N tend toward normal, but there is temperature sensitivity
for suppression of wing nicks (Foster, 1975; Portin, 1975).
Ax9 complements every recessive visible on the Notch map at 18
to 29 (Portin, 1977, Hereditas, 87: 77-84); with Ax59b and
Ax59d, it is semilethal. Negative complementation is eliminated by Dp(1;2)51b and results in a strong Ax phenotype
(Portin, 1975). The fate map for negatively complementing
heteroallelic Ax9/AxE2 suggests a focus of lethality in tissue
close to hypodermal sites of central thoracic structures; in
surviving gynandromorphs, negative complementation for morphological defects is autonomous (Portin, 1977, Genetics,
Homozygotes resemble Ax1. Ax16 is less fertile than
alleles AxE2, Ax71d, and Ax9 (Portin, 1975), and temperature
sensitive for the bristle and wing effects of Ax (Foster,
1975). In heterozygotes with Notch, Ax is expressed and the
Notch wing effect is enhanced (Foster, 1975; Portin, 1975).
At 29, heterozygotes with N are lethal. In Ax16/N264-40
heterozygotes, the TSP for lethality is in the second instar,
and for Ax-morphological effects, it is in the third instar
(Foster, 1973, 1975). In heterozygotes with recessive visibles at Notch, all are complementary at 18 and 25; at 29,
there are mild indications of noncomplementarity with nd and
nd2 (Portin, 1977). Heteroalleles Ax16/AxE2 and Ax16/Ax71d
are viable (Foster, 1975; Portin, 1975); Ax16/AxE1 is inviable
(negative heterosis) and heterozygotes with Ax9 and Ax1 are
lethal (negative complementation) (Foster, 1975; Portin,
1975), but Dp(1;2)51b restores viability (Portin, 1977).
Heterozygotes with the lethal alleles Ax59b and Ax59d are
lethal and mostly inviable upon the addition of Dp(1;2)51b
(Portin, 1975, 1977).
Homozygotes and hemizygotes semilethal at 22;
lethality approximates 100% at 25. Lethal in heterozygotes
with N mutants but viable and fertile with recessive visibles
at Notch. Ax59b/Ax59b; Dp(1;2)51b/+ are poorly viable and
infertile, and mutant phenotype is enhanced. Ax59b/+;
Dp(1;2)51b/+ females have diminished mutant expression compared to Ax59b/+ females which in turn are similar to males
Ax/Y; Dp(1;2)51b/+. In heterozygotes with spl at 25, the eye
is reduced in size but is larger than in spl/spl, and eye
roughness varies from very mild to undetectable. The report
by Welshons that Ax59b/spl did not express the split phenotype
was an error caused by uncontrolled temperature variation. In
cis heterozygotes, spl Ax59b/++, expression of split is
enhanced compared to Ax59b/spl; the eyes are rough and reduced
in size. No such enhancement is seen when fag is coupled to
Ax59b, and in Ax59b/fag, the expression of the recessive is
very mild and frequently nonpenetrant (Welshons, 1971). Ax59b
is semilethal with Ax9 and lethal with alleles Ax16, AxE2,
Ax71d, Ax1, and the addition of Dp(1;2)51b to heterozygotes of
Ax59b with Ax9 and Ax1 restores viability (Portin, 1975). The
temperature sensitivity of the Ax59b phenotype is strongest at
25; mutant expression decreases at both 18 and 29, with the
least mutant expression at 29 (Portin, 1981, Hereditas
94: 93-98). At 18, there is complementarity with all recessive visibles at Notch and strong Ax expression in every case
except when heterozygous with fag. At 29, all heterozygotes
are noncomplementary with the exception of nd; Ax expression
is diminished. At 29, homozygotes or hemizygotes with
Dp(1;2)51b are more viable than at 18 or 25 (Portin, 1977).
At 25, wing-vein interruption and bristle loss increases with
an increased dose of the mutant gene (Portin, 1981, Hereditas
95: 247-51). Somatic crossing over yields twin spots on
cuticular surface of flies, indicating that Ax59b is not a
primary cell lethal (Portin, 1980).
Homozygous, viable, phenotype like Ax1. Viable with
alleles AxE2 and Ax16, and lethal with Ax1 and Ax9 (negative
complementation), but viability restored by Dp(1;2)51b. There
is no obvious effect on the Notch phenotype in heterozygotes
with N8 or N55e11, but Ax phenotype is expressed. In heterozygotes with AxE2, the mutant phenotype is weakly expressed;
heterozygotes with lethal alleles Ax59b and Ax59d are lethal.
Ax71d is complementary with recessive alleles at Notch at 18,
25, and 29. The mutant expression of Ax tends to increase
with increasing temperature except that Ax71d/nd2 at 29 has no
Recessive lethal like alleles Ax59b and Ax59d.
Ax75c/+ is temperature sensitive for pleiotropic effects; the
variation in mutant expression with temperatures of 18, 25,
and 29 resembles that of Ax59b and Ax59d with some variation
in detail (Portin, 1981, Hereditas 94: 93-98). The Ax mutant
phenotype increases with increasing dose of the allele (Portin, 1981, Hereditas 95: 247-51).
AxE1/+ females at 20.5 have gaps in wing veins and a
reduction in number of ocellar and postvertical bristles.
Semilethal as hemizygote or homozygote. Heterozygotes
AxE1/Ax9 are viable and phenotypically
intermediate: AxE1/AxE2 and AxE1/Ax16 are inviable (negative
heterosis). AxE1 is inviable with most N mutants, but heterozygotes with N264-103 (a temperature-sensitive mutant) survive
at 22 but not at 29.
Homozygous viable, phenotype like Ax1. Temperature
sensitive for morphological phenotypes (Foster, 1975) but
stable for viability (Portin and Siren, 1976). Viable in
heterozygotes with N; Notch-wing phenotype is enhanced. At 18
and 25, complementary in heterozygotes with recessive alleles
at Notch; at 29, spl and nd2 are weakly expressed (Portin,
1977, Hereditas 87: 77-94). Heterozygotes fano spl AxE2/+++
are like spl/spl with suppression of wing-vein gaps; fano++/+
spl AxE2 and +spl AxE2/+++ show mild expression of spl
(Foster, 1975). AxE2 is viable with alleles Ax71d and Ax16;
lethal with lethal alleles Ax59b and Ax59d and with AxE1, Ax9,
and Ax1 (Foster, 1975; Portin, 1975), and the lethality with
Ax1 is more pronounced at 29 (Portin and Sir'n). In AxE2/Ax1,
the TSP for lethality is monophasic from the end of the third
instar to early pupa (Portin and Sir'n, 1976). In AxE2/Ax9,
the focus of lethality is close to hypodermal sites of ventral
thoracic structures, and in surviving gynandromorphs, the
negative interaction between alleles is autonomous (Portin,
1977, Genetics 86: 309-19).
Male lethal, mutant phenotype similar to Ax1.
Lethality is covered by Dp(1;2)51b and Dp(1;2)w64d, and males
with the duplication show the Ax phenotype. When lethality is
covered by w+Y, males have normal wing venation but lack ocellar bristles. In heterozygotes with fal2, females survive
exhibiting a strong Ax phenotype and rough eyes.
Male and female homozygotes lethal. AxS/+ males and
females show sparse thoracic hairs. AxS/Ax similar to Ax/Ax,
viability strongly reduced. AxS/NS is lethal. Not suppressed
Ax phenotype 100% penetrant in heterozygotes at 18
and 29; homozygous lethal at 29 and semilethal at 18. Surviving homozygotes have a stronger Ax expression than in heterozygotes. Lethal with N mutants at 29 and semilethal with
Ax59d. Ax in phenotype and complementary with recessive visibles at Notch at 18 and noncomplementary at 29.
Co: Confluens (W.J. Welshons)
Edith M. Wallace, unpublished.
Veins irregularly thickened, especially toward tips,
which are usually deltas and fused broadly to marginal vein.
Stronger expression in males than in females. Co/N8 wild type
except for slightly thicker L3 vein. Co/Ax like Ax/+. RK1A.
fa: facet (W.J. Welshons)
Facet mutants affect the texture of the eye and in
some cases cause slight to moderate wing nicks. Until now
some recessive mutations with wing nicking but with normal eye
texture have been designated as alleles of fa based upon their
not being complemented by N mutants; in this treatment their
designations have been changed to nd: notchoid, since they
fail to complement nd mutants and like nd alleles, they complement fa alleles. All fa alleles complement spl, another
eye-texture mutant in the N locus.
Eyes of all males moderately rough owing to irregularity in size, shape, and arrangement of facets. Not dosage
compensated; eyes of females less rough than those of males
with about 10% overlap of wild type. Eye roughness of the
females varies from nearly normal at 18 to marked at 29; pupal
stage temperature sensitive (Shellenbarger and Mohler, 1975,
Genetics 81: 143-62). Eye abnormality caused by overgrowth
of secondary pigment cells, which compresses cones and causes
overlying corneal facets to bulge (Waddington and Pilkington,
1942, DIS 16: 70). Wings have apical nicks in 0.25% of males
and 0-5% of females. N/fa1 has rough eyes of fa1 as well as a
Eyes equally rough in both sexes; wings not notched.
Eyes rougher than in fa males but not glossy as in fag;
heterozygotes fa3/fag are rough, not glossy (Welshons).
*fado-vg: facet-dominigene for vestigial
By itself, it is wild type. fado-vg/fa1 shows rough
eye character of fa1. fado-vg/fado-vg; vg/+ produces some wing
notching. Presumed by Goldschmidt to enhance dominance of vg
and thus termed a "dominigene". RK3.
Strong echinus-like eyes, darkening with age with
glistening frosted appearance. Homozygous females sterile,
but sterility may be separable from fafx (Kaplan and Hayes,
1967, DIS 42: 38).
Eyes have facets more irregular than fa, but surface
is smoothed, giving a glossy effect. Equal mutant expression
in both sexes. Pigment distribution may be uneven, contributing to an impression of altered eye color. No wing effect.
Eyes of fag/fa1 intermediate between the two homozygotes.
Complementary with spl, fano, nd, and nd2 (Welshons, 1965,
Science 150: 1122-29). RK1.
Large, rough eye with semiglazed surface and irregular pigment distribution causing a patchy red color. About
2/3 flies have incisions of the inner wing margin. Viable and
fertile as a male, reduced fertility in females (Fahmy, 1958,
DIS 34: 49).
Like fag and cannot be distinguished from it. In
heterozygotes with N mutants and in fag62/fag, the fag phenotype is exhibited; fag62/fa1 has a fa1 phenotype, and
fag62/spl is wild type.
fal/fa1 resembles fa1/fa1; not notched. Homozygous
A male-lethal allele of Notch. Females nearly wild
type but show occasional slight traces of Notch. Full complementation with spl but interacts with fag showing rough irregular eyes.
In males, eyes are rough with a variable tendency to
be glossy; with fag and fag62, eyes are very rough, but mutant
condition is not as extreme as that found in homozygous
glossy-eyed mutants. In heterozygotes with fa1, eyes are
slightly rough, overlapping wild type; with spl, the eyes are
The faswb allele, like fa1, is not dosage compensated, and
the mutant condition is poorly expressed in females.
faswb/fano has slight deltas at junction of longitudinal veins
with marginal veins; faswb
complements nd and nd2; and in heterozygotes of faswb, N55e11
and N264-40, the eyes are glossy and the Notch phenotype is
enhanced, resulting in reduced viability and fertility; with
the temperature-sensitive N60g11, heterozygotes are less
mutant, viable, and fertile. In double mutants, faswb fag,
the males have fag-like eyes; and wing veins are thickened and
delta like at tips; they resemble fano males except that wings
are seldom notched. The wing-venation effect is less extreme
in homozygous females (Welshons and Keppy, 1975, Genetics
80: 143-55; Keppy and Welshons, 1977, Genetics 85: 497-506).
l(1)N: lethal (1) Notch (W.J. Welshons)
There are four phenotypic varieties of l(1)N
alleles: (1) Those that are lethal with N and wild type with
the recessive visibles [see l(1)N1]; (2) Those that are lethal
with N but not wild type with the recessive visibles [see
l(1)N2, l(1)N3]; (3) Alleles whose heterozygotes with N+ have
a phenotype not recognized as Notch [see l(1)NB], or (4)
Alleles that are temperature sensitive for lethality and do
not express a Notch phenotype in heterozygotes with N+ [see
l(1)Nts]. The embryological defects in l(1)N1 are related to
those in N; the development in l(1)NB is sufficiently normal
to escape embryonic lethality (Poulson, 1967, 1968).
l(1)N1/+ females are wild type; l(1)N1/N females and
l(1)N1/Y males are lethal; l(1)N/Y;Dp(1;2)51b males are Co-like. Heterozygotes with recessive visibles at Notch are wild
type. Developmental defects in l(1)N1/Y males are more limited than in N/Y males and the defects are confined to the
anterior ectoderm (Poulson, 1967; 1968). Like N mutants,
l(1)N1 mutants are defective as embryos (Shellenbarger and
Mohler, 1975, 1978).
l(1)N2/+ females are wild type; l(1)N2/N females and
l(1)N2/Y males are lethal. Heterozygotes with fa and fag are
fa-like; with nd, they have nd-like wings and small eyes; with
nd3, they are viable, fertile and nd3-like. Developmental
defects in l(1)N2/Y males and time of lethal effect same as in
l(1)N1/Y. Some l(1)N2/l(1)Nts1 females survive to late pupal
stage (Shellenbarger and Mohler, 1975).
l(1)NB females have small eyes, fewer mesonotal
bristles, and, sometimes, bald areas on the thorax (Welshons,
1965). The dominant bristle effect is more extreme in
l(1)NB/Y;Dp(1;2)51b males than in l(1)NB/+ females. Heterozygotes with fa have fa-like eyes and, frequently, nicked wings;
with nd, they show notched wings and thickened veins; with
nd3, they are viable, fertile, and fa-like. l(1)NB/Y males
die during early larval life (Poulson, 1967). l(1)NB/l(1)Nts1
females die before pupation (Shellenbarger and Mohler, 1975).
Bristle effect autonomous in l(1)NB cells; homozygous mutant
cells survive in mosaics (Arnheim, 1967).
l(1)N69e/l(1)N69e and l(1)N69e/Df(1)N-8 females are
lethal at 18 and 29; l(1)N69e/+ heterozygotes are almost
always wild type. l(1)N69e homozygotes die before pupation,
but l(1)N69e/l(1)Nts1 heterozygotes survive until the pupal
l(1)Nts1/+ females are wild type at 18 and 29, while
l(1)Nts1/Df(1)N-8 females are lethal at 29, but a few escapers
are found at 18. l(1)Nts1 homozygotes are viable at 18, but
lethal at 29. If homo- and hemizygotes kept at 18C until
eclosion are transferred to 29C and kept at this temperature
for six days, they gradually become flightless and show gross
histological changes in the flight muscles (Vikki and Portin,
1987, William Roux's Arch. Dev. Biol. 196: 12-15). Heterozygotes show recessive visible defects at 18, but not at 29.
l(1)Nts1/l(1)N2 and l(1)Nts1/l(1)N3 females survive until the
late pupal stage at 29. When heat pulses are given to pupae
prior to sensillum-precursor-cell-determination, extra sensilla are produced; when given after sensillum-precursor-cell
determination, the precursor cells form neurons only, not
accessory cells (Hartenstein and Posakony, 1990, Dev. Biol.
Similar to l(1)Nts1 except for occasional survival
of homozygotes to the pupal stage at 29 and weaker expression
of recessive visible defects in heterozygotes at this temperature.
Mohr, 1924, Z. Induktive Abstammungs-Verebungslehre 32: 118.
Mutant alleles are characterized by the following
types of expression: Wings of heterozygotes incised at tips
and often along edges; veins L3 and L5 thickened; thoracic
microchaetae crowded and irregularly distributed (Mohr, 1919,
Genetics 4: 275-82; 1923, Z. Indukt. Abstamm. Vererbungsl.
32: 108-232). Males and homozygous females are lethal. In
some N mutants, the phenotype is mild and varies in one or
more of its typical features, but such N's can usually be
identified by phenotypes expressed when heterozygous with
recessive visible eye and wing mutants that also occur at
Females N/N+ are Notch; females N/N+;Dp(1;2)51b (representing a duplication for the Notch locus) are wild type. In the
hemizygous male, N/Y is lethal, whereas N/Y;Dp(1;2)51b is
viable and phenotypically normal; the wild phenotype is dependent upon the presence of the normal dosage of 3C6-7 for each
sex. An extra dose of 3C6-7 [as in Dp(1;2)51b or Dp(1;1)Co]
causes the expression of the dominant phenotype Confluens
(Co); thus N+/N+;Dp(1;2)51b females and N+/Y;Dp(1;2)51b males
are Co-like (Welshons, 1965). Deficiency mapping places Co to
the left of N (Merriam).
Homozygotes and hemizygotes for all N mutants suffer the
same embryological defects. In developing embryos, the pattern of differentiation of anterior and ventral embryonic
ectoderm is aberrant; both presumptive hypoderm and presumptive neuroblasts develop as neuroblasts, resulting in embryos
with a hypertrophied central nervous system lacking ventral
and ventral-lateral hypoderm [Poulson, 1939, DIS 12: 64-65;
1940, J. Exp. Zool. 83: 271-325; 1950, Biology of Drosophila
(M. Demerec, ed.). Wiley, New York, pp.168-274; 1967, DIS
42: 81; Wright, 1970, Adv. Genet. 15: 305-15]. Sensillum
differentiation in peripheral nervous system of embryos also
abnormal (Hartenstein and Campos-Ortega, 1986, Roux's Arch.
Dev. Biol. 195: 210-21). In mosaic embryos (N/N+ and N/0
cells), the N/0 cells never give rise to hypoderm within the
neurogenic region (Hoppe and Greenspan, 1986, Cell 46: 773-83). However, single N/0 cells transplanted to N+ recipient
embryos can give rise to hypoderm (Technau and Campos-Ortega,
1987, Proc. Nat. Acad. Sci. USA 84: 4500-04).
Wing-notching weak and rarely visible.
N264-66/fa heterozygotes variegate for fa. Some
N264-66/Y males are viable and have cream-colored eyes with
spots of normal red pigment.
A weak Notch. Deltas on wing veins are most reliable character for classification. Lethal when heterozygous
with nd3, N60g11, and NCo. In homozygotes and hemizygotes
hyperplasia of central nervous system extreme; embryonic peripheral nervous system abnormal with sensilla undifferentiated
(Hartenstein and Campos-Ortega, 1986, Wilhelm Roux's Arch.
Dev. Biol. 195: 210-21).
Wings seldom notched; veins thickened; deltas at
tips. N60g11/+ heterozygotes have normal eyes at 29 and a
disrupted facet arrangement at 21. With increasing temperature, rough eye phenotype diminishes and Notch mutant characteristics are expressed. TSP for disrupted facets is in the
third instar. N60g11/N60g11 Dp(1;2)51b7 females are viable at
29; survival sharply decreased at 20-23; TSP for lethality in
middle of embryonic stage. N60g11/fa flies have eyes like fa.
Semilethal with nd3. Viability poor with nd.
Typical Notch. N64d6 spl flies cannot be distinguished from N64d6 spl+ flies. When spl is coupled to
N64d6, spl is not enhanced by E(spl).
The Notch inversion N66h26 (synonym:
In(1)w8xN66h26), with breakpoints in w and N, was derived from
Df(1)N-8 and is unstable in crosses involving a wafagrb stock,
giving rise to N+ revertants such as w8x1N+ and w8x2N+
(Welshons and Keppy, 1981; Grimwade et al., 1985). Recombination hetween w and N, which does not occur in N66h26, does
take place in these reversions, indicating that reversion to
N+ is accompanied by reinversion of In(1)N66h26. The w8x1N+
derivative of N66h26 is also unstable in crosses involving the
wafagrb stock, generating (stepwise) various mutant and wildtype Notch alleles (Grimwade et al., 1985). Df(1)w79, another
derivative of N66h26, is deficient for both N and w (Welshons
and Keppy, 1981).
Typical Notch. N68j/+ females have wings excised at
the tips; N68j/spl females are spl. N64j flies carrying
Dp(1;1)Co are almost wild type. Mutant males with w+Y are
viable (Hayman and Maddern, 1969).
Typical Notch. N68j1/Df(1)N-8 females are lethal at
29 and 18; Notch-wing phenotype shows little or no response to
temperature (Shellenbarger and Mohler, 1975).
Shows variable Notch-wing expression depending on
temperature. Lethal in homozygotes and in heterozygotes with
Df(1)N-8 at 29 and 18. N69c/+ heterozygotes show greater
expression of Notch-wing at 18 than at 29 (Shellenbarger and
Typical Notch. Genetically unstable, giving rise
spontaneously to six independent N+ revertants. The N+10
revertant is rather unstable (Grimwade et al., 1985).
Typical Notch. Male embryos show developmental
abnormalities like those of Df(1)N-8 (Poulson, 1939). Lethal
Typical Notch. Male embryos show developmental
abnormalities like those of Df(1)N-8 (Poulson, 1939). Lethal
Temperature-sensitive Notch allele.
N264-103/nd3 females are viable at 22o and lethal at 29o, with
a long, possibly polyphasic, TSP beginning in the embryonic
stage. N264-103/spl females show eye-facet disarray, notching, bristle-number variation, and tarsal-segment fusion, the
TSP being in the third instar (Foster, 1973). N264-103/spl
variegates for spl; N264-103/fa is fa.
Typical Notch except for semilethality with nd3.
Wing tips seldom notched; veins thickened, with deltas. Acrostichal rows irregular. NCo/nd3 heterozygotes
lethal; rare survivors sterile and weak. NCo/+ females show
thickened wing veins (a Confluens-like phenotype) more frequently than nicked or notched wings. Also, NCo heterozygous
females with an extra dose of 3C6-7 [Dp(1;1)Co or Dp(1;2)51b]
or hemizygous males with Dp(1;2)51b have an enhanced
Confluens-like wing phenotype.
Typical Notch. Lethal with nd3.
Wings notched at tips and occasionally at sides;
veins thickened, with deltas. Eyes slightly smaller than normal; occasionally one eye extremely small.
Typical Notch. Lethal with nd3. Cell lethal in tergites and dorsal mesothorax (Ripoll and Garcia-Bellido, 1979,
Genetics 91: 443-53).
Weak Notch. NS/AxS is lethal.
nd: notchoid (W.J. Welshons)
Wings notched and veins thickened. The notching is
found mostly on anterior and posterior margins and is the
result of cell death (Thompson and Spivey, 1984, Genet. Res.
44: 201-69). Homozygotes are viable and fertile in both
sexes. N/nd1 heterozygotes are partially viable and relatively
infertile (Portin, 1977) and show notched and straplike wings
and small eyes. About 10% of fa/nd1 flies have small notches
in one or both wings. nd3/nd1 heterozygotes have slightly
thickened wing veins with deltas; spl/nd1 heterozygotes lack a
few bristles (like spl/+) and their eyes are sometimes smaller
than normal and roughened. spl nd1 males have rough eyes,
nd-like wings, and irregular, bushy sex combs.
nd0 (= fan)
From Glass, 1933, J. Genet. 27: 233-41.
Wings have apical nicks or notches in 90-100% of
males, but only 8% of homozygous females. Eyes not rough.
fa/nd0 is wild type. Viability and fertility excellent. RK2
nd1 is temperature-sensitive. In homozygotes at 29,
the eyes are rough and reduced in size, there is extreme wing
notching, and wing veins are thick; at 25, the abnormalities
are less severe, and at 18, the eyes are normal and the wings
are nicked. At 29, heterozygotes with fa, fag, and spl are
complementary (Foster, 1973; Shellenbarger and Mohler, 1975).
nd1/Y;E(spl)r19/+ males have severely reduced and crumpled
wings (Xu, Rebay, Fleming, Scottgale, and Artavanis-Tsakonas).
Wing development also affected in nd1/Y;mam10/+ males. nd1
and mam10 double heterozygotes are wild type. Wing notching
is suppressed in nd1/Y males by Dl/+.
nd2/nd2 and nd2/nd1 flies resemble nd1 homozygotes;
nd2/nd3 heterozygotes are noncomplementary (Welshons). The nd2
allele is temperature sensitive; in homozygotes at 29, the
eyes are small and rough (spl-like), wings have extreme
notches, wing veins are thickened, tarsi are shortened, and
the mutants are semilethal as late pupae; at 25, the abnormalities are much less severe; at 18, the eyes are slightly spl-like, wings are nicked, wing veins are incomplete, some bristles are missing, and the mutants are semilethal as late
pupae. At 29, fa/nd2 heterozygotes have nicked wings, spl/nd2
heterozygotes are spl-like, and nd4/nd2 heterozygotes resemble
N/+ (Shellenbarger and Mohler, 1975). Similar wing abnormalities in nd1/Y;E(spl)r19/+ and nd2/Y;E(spl)r19/+ males. The
temperature-sensitive rough-eye phenotype of nd2 is enhanced
by E(spl)/+ (Xu et al.).
Wings of both sexes notched at ends of L3 and L4
veins; wing veins enlarged and delta-like at tips. Mild
mutant expression often limited to wing-vein effect. Mutant
expression diminished at high temperature (Shellenbarger and
Mohler, 1975, Genetics 81: 143-62). Heterozygotes show
extremely weak dominance. nd3/N almost completely lethal;
survivors are sterile and have an exaggerated Notch phenotype.
nd3/fa closely resembles wild type. Heterozygotes with fag
and spl are complementary; with nd and nd2, heterozygotes are
noncomplementary with a mild mutant expression of nd3-like
wings. Up to 5% of nd3 males from aged cultures show hyper- and hypodeveloped external genitalia (Kroeger, 1960, J. Morphol. 107: 227-32).
Viable when homo- or hemizygous; shows adult wing
nicking. Lethal when heterozygous with N deficiencies.
Phenotype similar to nd.
Wild-type revertant of nd3.1072. Viable in combination with N deficiencies.
Temperature sensitive and semilethal in homozygotes;
wing phenotype more extreme and survival greater at 18 than at
29. nd4/+ lethal at both temperatures.
Like ndts69j (see below).
Like ndts69j (see below).
Temperature-sensitive semilethal. Homozygotes
express weak notches, mild deltas, and extra bristles at both
18 and 29; both homozygotes and hemizygotes show significantly
better survival at 18 than at 29. ndts69j/+ heterozygotes
have normal wings at 18 and 29. Df(1)N-8/ndts69j heterozygotes have significantly better survival at 18 than at 29.
In general, ndts70j homozygotes and heterozygotes
resemble the other Nts mutants. ndts70j homozygotes, however,
are wild type at 18 and some ndts70j/+ heterozygotes have
notched wings at 29.
In homozygotes, eyes are rough and small, bristles
are often doubled or split (sometimes missing). Hemizygotes
show a more extreme reduction in eye size as well as an
increase in facet and bristle abnormalities (Shephard et al.,
1989). Both eye and bristle abnormalities occur at all temperatures from 18 to 29, an exception being a spl stock from
Novosibirsk, Russia, that shows temperature sensitivity
(Mglinetz, 1980, DIS 55: 107-08). The bristle phenotype is
caused by an extra division of an initial bristle-forming cell
(Lees and Waddington, 1943, Proc. R. Soc. London, B 131: 87-110; Van Breugel and Van der Aart, 1979, Dev. Biol.
186: 267-71). A few bristles (sockets remaining) are usually
removed from the posterior border of tergites in spl/+ heterozygotes (Welshons). The eye abnormalities are the result of
abnormal differentiation of photoreceptors at the morphogenetic furrow (Cagan and Ready, 1989). Heterozygotes with
the other recessive visibles at Notch are almost normal except
for spl/nd2 flies; the latter are spl-like at 29 (Shellenbarger and Mohler, l975). Another temperature-sensitive
effect is shown by N264-103/spl flies, which have abnormal eye
facets at 28-29 but are almost wild type at 20-22 (Foster,
1973, Dev. Biol. 32: 282-96). The spl phenotype can be
enhanced by E(spl)/+ or E(spl)/E(spl). spl/+;E(spl)/+ flies
resemble spl/spl flies; spl/spl; E(spl)/+ and spl/Y; E(spl)/+
flies show a very extreme mutant phenotype (Shephard et al.,
1989). spl/Y;E(spl)R19/+ males and spl/+;E(spl)R19/+ females
show spl and Ax-like phenotypes (Xu et al.). The spl phenotype is reduced in mam heterozygotes. When, however, spl is
coupled to a N point mutant, as in N64d6 spl/+ +;E(spl)/+, the
phenotype is not spl (Welshons, 1971) split behaves autonomously in mosaics in regard to both eye and bristle phenotypes (Stern and Tokunaga, 1968, Proc. Nat. Acad. Sci. USA
60: 1252-59). The spl phenotype becomes dominant if spl is
coupled, in cis, to lethal Ax alleles. Thus Ax spl/++ is spl,
while +spl/++ is wild type (Welshons, 1971; Kelley et al.,
Resembles spl except for smaller eyes.