su(f): suppressor of forked
su(f) mutations are found with several levels of
reduced expression, and some if not all mutant alleles are
sensitive to temperature. The weakest exhibit no phenotype
when raised at 25 other than modification of the expression of
specific alleles at other loci; increasingly reduced expression leads to a specific phenotype, which variably includes
Minute-like bristles, rough eyes with some anterior indentation, reduced or absent ocelli, missing ocellar and other head
and thoracic bristles, irregular acrostichal rows, excessive
melanization, especially on head, and some crippling of legs;
also wings may be blistery, broader, with extra veins and may
be held upward and outward (Grell, CP627; Schalet, 1968, DIS
44: 125). The most severely affected alleles are lethal, the
lethal period becoming earlier with increasing severity. At
least one instance of interallelic complementation has been
reported by an allele which in surviving adults exhibits pale
yellow thread-like chaetae. Viable alleles act as allele-specific but locus-nonspecific modifiers. The locus was
recognized by the nearly wild-type bristle phenotype of
f su(f); some bristles slightly shortened or twisted at tips.
Autonomous in gynandromorphs. f alleles fall into two
classes: suppressible (f1, f4, and f5) and insuppressible (f3
and f3N)(Green, 1959, Heredity 13: 303-15). Suppressible
alleles are spontaneous and contain insertions of transposable
sequences; such alleles are also frequently modified by mutations in other modifier genes. For example, among alleles
with gypsy inserts, su(f) suppresses ctk, lz1, f1, f5, bx34e,
but not y2, Hw1, sc1, or ct6; all are suppressed by su(Hw).
In addition, su(f) enhances the spontaneous mutants wa (copia)
and lz37, but not we, lz34, lzk, s1, or v1 (412); all of these
are affected by one or more other suppressor genotypes
(Rutledge, Mortin, Schwarz, Thierry-Mieg, and Meselson, 1988,
Genetics 119: 391-97). Does not suppress the effect of f on
the phenotype of dvr, i.e. crumpled wings (Lee, 1974, Aust. J.
Biol. Sci. 27: 305-7).
Wild type in appearance with normal viability and
fertility when raised at 25; however, both su(f) flies raised
at 29-30 and su(f)/Df(1)su(f) flies raised at 25 display the
Minute-like syndrome. The same phenotype is seen in combinations with su(f)2 and su(f)6 raised at 29. su(f)/Df(1)su(f)
is lethal when raised at 29; viability also temperature sensitive in combination with su(f)3 and su(f)5 (Schalet and
Lefevre, 1976). su(f) enhances wa; wa su(f) eyes nearly white
at 25 and white at 18 but apricot in flies raised at 29;
suppresses lz1 and enhances lz37 at all temperatures.
Increases the accumulation of gypsy transcript, suggesting
that the wild-type allele represses gypsy (Parkhurst and
Corces, 1986, Mol. Cell. Biol. 6: 2271-74); protein binding
to a negative regulatory sequence of gypsy is reduced in
nuclear extracts from su(f) pupae compared with those from
wild type, again suggesting gypsy repression by su(f)+ (Mazo,
Mizrokhi, Karavanov, Sedkov, Krichevskaha, and Ilyn, 1989,
EMBO J. 8: 903-11).
Homozygotes lethal at the larval stage; homozygous
germ-line clones don't survive; no effect on development of
peripheral or central nervous systems (Perrimon, Smouse, and
Miklos, 1989, Genetics 121: 313-31). Survives and suppresses
f in combination with su(f)1 at 25, and exhibits M-like syndrome in flies raised at 18. wa displays dilute apricot pigmentation in su(f)1/su(f)2 flies raised at 25 but white eyes
when raised at 18 (Schalet and Lefevre, 1976). su(f)2 shown
to be proximal to su(f)1 by recombination (Schalet).
Homozygous lethal. Fails to complement lethality of
either su(f)3 or su(f)5. In combination with su(f)1 shows the
M-like syndrome at 25 and is lethal at 29.
May be the only pale-bristle allele. One other
allele of this type was found by Dale Grace as a sex-lined
lethal (Schalet). Recovered originally as a sex-linked recessive lethal, but fully viable, though weak, and suppresses f
when raised at 18. Survivors exhibit pale-yellow, thread-like
bristles, darker pigmentation dorsoanteriorly on thorax, and
curled or wrinkled wings. Lethality at late pupal stage;
homozygous germ-line clones show no maternal effect; also, no
zygotic effects on development of peripheral or central nervous systems (Perrimon, Smouse, and Miklos, 1989, Genetics
121: 313-31). Interactions of su(f)4 with other su(f)
alleles are as follows: su(f)1, same as su(f)1 homozygotes at
all temperatures; su(f)2, complementation for viability and
bristle color and slight complementation for suppression of f;
su(f)3, lethal at the time of puparium formation at 25, fully
viable with some chaetae of all individuals showing the pale-bristle phenotype and the texture of the wings appearing
abnormal at 18; su(f)5, fully viable and normal at 18, variable viability with a broad streak of dark pigment on thorax,
which sometimes is concentrated at dorsal anterior region, and
wings which may extend upward and outward at 25, lethal prior
to puparium formation at 29; su(f)6, fully viable and normal
at 18 and 25 but exhibiting the M-like syndrome at 29;
Df(1)su(f), lethal at the time of puparium formation at 25 and
just prior to eclosion at 18. Enhances wa; wa su(f) eyes
white in flies raised at 25 and dilute apricot at 18; also
enhances lz37 at 18.
Homozygotes lethal at the larval stage; homozygous
germ-line clones don't survive; no effect on development of
peripheral or central nervous systems (Perrimon, Smouse, and
Miklos, 1989, Genetics 121: 313-31). Lethal with su(f)3 at
25 and with su(f)4 at 29. In combination with su(f)1,
displays the M-like syndrome at 25 and lethal at 29.
The first allele recovered specifically as a
temperature-sensitive lethal; completely lethal at 29;
suppresses f at 25 but not at 18. Temperature-sensitive
period for lethality from 50 to 140 h after oviposition, for f
suppression coincident with bristle differentiation. Shift up
to 30 before end of the second instar causes failure to
pupariate; full-sized third instar larvae produced, which live
10-14 days; salivary-gland-secretion proteins specifically
reduced or absent in these larvae, although the associated
chromosome puffs appear normally; other proteins unaffected
(Hansson, Lineruth, and Lambertsson, 1982, Wilhelm Roux's
Arch. Dev. Biol. 190: 308-12); shift up prior to 70 h leads
to little or no accumulation of Sgs transcripts as detected in
Northern blots probed with sequences from Sgs3, Sgs4, Sgs7,
and Sgs8, whereas a 48-h pulse beginning at 75 h is without
effect on transcription or translation of Sgs genes (Hansson
and Lambertsson, 1983, Mol. Gen. Genet. 192: 395-40). Shift
up to 30 in early third instar blocks the increase in ecdysterone titer normally occurring at the end of L3; ecdysterone
supplementation induces abortive pupariation and stimulates
prepupal polypeptide synthesis (Hansson and Lambertsson, 1984,
Wilhelm Roux's Arch. Dev. Biol. 193: 48-51); leg discs of
such larvae unable to evert, either in vivo or in vitro (Fekete and Lambertsson, 1980, Hereditas 93: 169-76). Homozygous
females raised under permissive conditions, when shifted up to
30 cease laying eggs and the ovarian oocytes degenerate; fertility recoverable after pulses of three but not eleven hours
(Dudick et al.). Heterozygotes with Df(1)su(f) at 25, su(f)1
at 29, and su(f)3 at 30 exhibit the M-like syndrome. Enhances
M(3)67C, as indicated by reduced viability of su(f)8 versus
su(f)+ sibs that are M(3)67C/+ (Girton, Langner, and Cejka,
1986, Roux's Arch. Dev. Biol. 195: 334-37). Enhances gypsy
expression, more at 25 than at 18 (Parkhurst and Corces, 1986,
Mol. Cell. Biol. 6: 2271-74).
Recovered as a surviving son of su(f)3; still
suppresses f, but is no longer lethal. X/Y males survive and
have small rough eyes, broad outstretched wings and irregular
abdominal pigmentation; homozygous females usually lethal with
escapers showing the same phenotype as the males. XXY females
survive and resemble XY males. X0 males die. su(f)9/su(f)3
never survives. Attributed by authors to a recessive
variegated-position-effect suppressor of the lethality of
su(f)3; locates to proximal extremity of the X; complements
bb.
Selected as a cell-autonomous, temperature-sensitive
lethal. Relative survival is 85% at 22, 75% at 25 and 1% at
29; temperature-sensitive period from first larval instar to
early pupa. Homozygous females become sterile after two days
at 29, whereas males so treated remain fertile. 23% of eggs
laid at 29 fail to hatch; surviving larvae grow at subnormal
rate and survive for up to twelve days, reaching the third
instar; imaginal discs reduced greatly in size. 48-h pulses
of 30 during late second and third instars results in considerable cell death in imaginal discs with a consequent deletion
of some pattern elements and duplications of others in the
head and legs; head duplications occur only in association
with deficiencies; leg duplications seen as simply and complexly branched appendages involving variable numbers of
joints. Pulses applied to early pupae lead to failure of histoblast differentiation and applied later to the lack of chaetae (Russell, Girton, and Morgan, 1977, Wilhelm Roux's Arch.
Dev. Biol. 183: 41-59). Extensive use made of leg duplications induced in su(f)12 in investigations of pattern formation (Tiong, Girton, Hayes, and Russell, 1977, Nature
268: 435-37; Postlethwait, 1978, Wilhelm Roux's Arch. Dev.
Biol. 185: 37-57; Girton and Russell, 1980, Dev. Biol.
77: 1-21; Girton, 1981, Dev. Biol. 84: 164-72; Girton and
Russell, 1981, Dev. Biol. 85: 55-64). Enhances M(3)67C, as
indicated by reduced viability of su(f)12 versus su(f)+ sibs
that are M(3)67C/+ (Girton, Langner, and Cejka, 1986, Roux's
Arch. Dev. Biol. 195: 334-37).
A cell-autonomous, temperature-sensitive recessive
allele. Phenotype similar to that of su(f)12 except that
trypan-blue staining provides no evidence of cell death
resulting from heat shock at stages of development in which
such treatment induces leg duplications. Authors postulate
that su(f)12 discs developmentally impaired by heat shock,
giving rise to observed abnormalities. Temperature-sensitive
period from late second instar until two hours into pupariation. Shifts from 22 to 29 during the first larval instar
leads to inability to pupariate; shifts between 112 and 164 h
arrests adult development; shifts within the first six hours
after the temperature for lethality removes bristles from the
tergites. Gynandromorphs and somatic clones formed normally
at permissive temperatures, but are not observed in adults
produced at 29. Ecdysteroid level of larvae raised at 29 are
less than one-tenth that of wild type; pupariation can be
induced by ecdysterone supplementation (Klose, Gateff, Emmerich, and Beikirch, 1980, Wilhelm Roux's Arch. Dev. Biol.
189: 57-67).
Temperature-sensitive lethal allele. Temperature-sensitive period for lethality extends from the second larval
instar until twelve hours after pupariation. Shifting adult
females to restrictive conditions results in the gradual abolition of oviposition; during the first day normal appearing
eggs, many of which hatch, are produced, on the second day the
hatchability of the eggs is reduced, and by day four the eggs
are small and misshapen and lack chorions; oviposition ceases
on the fifth or sixth day after shift up; at this time the
ovary is deficient in stage 8-11 oocytes and lacks follicle
cells indicating a breakdown in vitellogenesis. Shift back
down to 25 leads to resumption of egg laying after four days.
Ovarian response is autonomous in ovarian transplants. Fertility of males irreversibly impaired by shift up to 29.
Homozygotes and hemizygotes survive at all temperatures from 18 to 29; complements the lethality of lethal
alleles. The suppression of f is temperature sensitive, but
the sensitivity is of opposite sign from that of other
temperature-sensitive alleles; f su(f)23 flies raised at 18
have suppressed forked bristles, whereas those raised at 29
are forked; the temperature-sensitive period sharply confined
to the short interval at which bristle development is initiated. Does not appear to enhance M(3)67C.
Similar to su(f)1; enhancement of wa, however, seen
only in su(f)1/su(f)24. Closely linked to or inseparable from
a variable recessive abnormality giving small misshapen eyes.
