FlyBase Allele Report: Dmel\if[k27e]

Slight irregularities in the apical surface of the salivary gland are seen at stage 12 in mutant embryos. By stage 14/15 the salivary gland tube is buckled.

(Ismat et al., 2013)

Adult if^k27e homozygous mutant intestinal stem cell clones have similar maintenance 7 days and 14 days after clone induction compared to control clones.

(Lin et al., 2013)

Homozygous embryos show axon guidance defects in the ISNb pathway (80.0% of hemisegments), in the SNa pathway (56.2% of hemisegments) and in the central nervous system (36.4% of hemisegments). The defects in the ISNb and Sna pathways are characteristic of increased fasciculation, while defects that are characteristic of both increased and of decreased fasciculation are seen in the central nervous system.

(Huang et al., 2007)

if^k27e dorsal branch terminal cell clones do not cause any detectable defects in terminal cell morphology.

(Levi et al., 2006)

Salivary cells appear to invaginate normally in homozygous embryos. The first group of salivary cells to be internalised reach the approximate level of the wild-type turning point (the point where salivary cells turn to reorient their movement posteriorly in wild-type embryos) but fail to migrate further. The remaining salivary cells continue to be internalised, and in late stage embryos the salivary tubes are frequently folded in half with the distal tips oriented anteriorly. Salivary tube length in the mutant embryos is similar to that of wild type in all stages of morphogenesis and salivary tube diameter in the mutant embryos is similar to that of wild type.

(Bradley et al., 2003)

Mutant embryos show loss of innervation of the muscle 6/7 cleft by the RP3 motorneuron (innervation is seen in only 28% of mutant hemisegments), often due to target bypass. Myopodia extending from muscle 6 are initially present at numbers similar to wild type (at 12 hours), but myopodia clustering can only be detected in 10% of hemisegments at 13 hours (compared to 46% of hemisegments in wild type).

(Ritzenthaler and Chiba, 2003)

if^k27e mutant embryos exhibit thinning of the longitudinal fascicles (visible with Fas2), with occasional defasciculation defects, along with a low frequency of midline crossover errors.

(Stevens and Jacobs, 2002)

Embryos exhibit normal epidermis and resultant secreted cuticle, defects lie in internal tissues. Somatic muscle detach and round up. Gut morphogenesis is defective: anterior midgut does not become a slender tube and only two fat gastric caecae are formed. The ventral nerve cord does not fully condense.

(Bloor and Brown, 1998)

Homozygous embryos have an increased rate of axon errors in the central and peripheral nervous systems compared to wild-type.

(Hoang and Chiba, 1998)

Embryos exhibit many abnormalities. Temperature shift experiments for higher levels of Scer\GAL4 expression suggest if expression is required early in wing development.

(Li et al., 1998)

Dorsal herniation is observed in homozygotes but not in double mutant combinations with mew^H7, mew^M6, mew⁴⁹⁸ and mew⁸¹. Clones in the eye do not exhibit photoreceptor disorganisation.

(Brower et al., 1995)

Larvae do not exhibit proventricular cell migration defects.

(Pankratz and Hoch, 1995)

Clonal analysis reveals that lack of if has no discernible effect on germ cell development. Mutant embryos show a distinct and reproducible separation between the ectodermal and mesodermal tissue layers of the germband, though the separation is not complete. Midgut primordia meet and initiate fusion at least 1 to 2 hours after wild type embryos would. Visceral mesoderm shows gaps and irregularities. Midgut constrictions partially form.

(Roote and Zusman, 1995)

Muscle attachment abnormality in embryo. Muscles 12, 8 and 4 are most often affected.

(Drysdale et al., 1993)

Heterozygotes with if³ exhibit a higher frequency of blistering.

(Wilcox et al., 1989)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

if^k27e has abnormal neuroanatomy phenotype, enhanceable by sli²

(Stevens and Jacobs, 2002)

Enhancer of

Statement

Reference

if^k27e is an enhancer of abnormal neuroanatomy phenotype of sli^unspecified

(Stevens and Jacobs, 2002)

NOT Enhancer of

Statement

Reference

if^k27e/if[+] is a non-enhancer of visible | dominant phenotype of sog^EP7

(Araujo et al., 2003)

if^k27e/if[+] is a non-enhancer of visible | dominant phenotype of sog^EP11

(Araujo et al., 2003)

Suppressor of

Statement

Reference

if^k27e/if[+] is a suppressor of viable phenotype of slow¹

(Gilsohn and Volk, 2010)

NOT Suppressor of

Statement

Reference

if^k27e/if[+] is a non-suppressor of visible | dominant phenotype of sog^EP11

(Araujo et al., 2003)

if^k27e/if[+] is a non-suppressor of visible | dominant phenotype of sog^EP7

(Araujo et al., 2003)

Other

Statement

Reference

Df(3L)Exel6083/+, if^k27e has abnormal neuroanatomy | dominant phenotype

(Huang et al., 2007)

if^k27e, sws^olfE-x26 has abnormal smell perception phenotype

(Ayyub and Paranjape, 2002)

if^k27e, mys^olfC-x10 has abnormal smell perception phenotype

(Ayyub et al., 2000)

if^k27e, mys^olfC-x17 has abnormal smell perception phenotype

(Ayyub et al., 2000)

if^k27e, mys^olfC-x3 has abnormal smell perception phenotype

(Ayyub et al., 2000)

if^k27e, mys^olfC-x5 has abnormal smell perception phenotype

(Ayyub et al., 2000)

Phenotype Manifest In

Suppressed by

Statement

Reference

if^k27e, mew⁴⁹⁸ has midgut primordium phenotype, suppressible by if^Δ.C.UAS/Scer\GAL4^how-24B

(Li et al., 1998)

if^k27e, mew⁴⁹⁸ has midgut primordium phenotype, suppressible by if^Δ.m8.UAS/Scer\GAL4^how-24B

(Li et al., 1998)

if^k27e, mew⁰²³ has midgut primordium phenotype, suppressible by if^Δ.C.UAS/Scer\GAL4^how-24B

(Li et al., 1998)

if^k27e, mew⁰²³ has midgut primordium phenotype, suppressible by if^Δ.m8.UAS/Scer\GAL4^how-24B

(Li et al., 1998)

Enhancer of

Statement

Reference

if^k27e/if[+] is an enhancer of larval somatic muscle cell phenotype of slow¹

(Gilsohn and Volk, 2010)

if^k27e is an enhancer of fascicle phenotype of sli^unspecified

(Stevens and Jacobs, 2002)

NOT Enhancer of

Statement

Reference

if^k27e/if^k27e is a non-enhancer of adult posterior midgut epithelium | somatic clone phenotype of mew^M6

(Lin et al., 2013)

if^k27e/if[+] is a non-enhancer of wing vein phenotype of sog^EP7

(Araujo et al., 2003)

if^k27e/if[+] is a non-enhancer of wing vein phenotype of sog^EP11

(Araujo et al., 2003)

NOT Suppressor of

Statement

Reference

if^k27e/if^k27e is a non-suppressor of adult posterior midgut epithelium | somatic clone phenotype of mew^M6

(Lin et al., 2013)

if^k27e/if[+] is a non-suppressor of eye phenotype of Atg1^K.GMR

(Chen et al., 2008)

if^k27e/if[+] is a non-suppressor of wing vein phenotype of sog^EP11

(Araujo et al., 2003)

if^k27e/if[+] is a non-suppressor of wing vein phenotype of sog^EP7

(Araujo et al., 2003)

Other

Statement

Reference

if^k27e/if[+], slow¹ has flight muscle cell phenotype

(Gilsohn and Volk, 2010)

Df(3L)Exel6083/+, if^k27e has larval intersegmental nerve phenotype

(Huang et al., 2007)

Df(3L)Exel6083/+, if^k27e has presumptive embryonic/larval central nervous system phenotype

(Huang et al., 2007)

Df(3L)Exel6083/+, if^k27e has larval segmental nerve phenotype

(Huang et al., 2007)

if^k27e, mew^M6 has terminal tracheal cell | somatic clone phenotype

(Levi et al., 2006)

if^k27e, mew⁴⁹⁸ has midgut primordium phenotype

(Li et al., 1998)

if^k27e, mew⁰²³ has midgut primordium phenotype

(Li et al., 1998)

if^k27e, mew⁴⁹⁸ has somatic muscle cell phenotype

(Roote and Zusman, 1995)

if^k27e, mew⁰²³ has somatic muscle cell phenotype

(Roote and Zusman, 1995)

if^k27e, mew^M6 has somatic muscle cell phenotype

(Roote and Zusman, 1995)

Additional Comments

Genetic Interactions

Statement

Reference

Reduced maintenance phenotype of adult mew^M6/mew^M6, if^k27e/if^k27e double mutant intestinal stem cell clones is partially rescued by expression of mew^UAS.cWa under the control of Scer\GAL4^Act.PU in these clones.

(Lin et al., 2013)

No significant overgrowth of the neuromuscular junction is seen in Fak^N30/Fak^KG00304 third instar larvae which are also heterozygous for if^k27e.

(Tsai et al., 2008)

if^k27e/+ ; Df(3L)Exel6083/+ double heterozygotes show axon guidance defects characteristic of increased fasciculation in the ISNb pathway (72.0% of hemisegments), in the SNa pathway (53.7% of hemisegments) and in the central nervous system (42.1% of hemisegments). These defects are not seen in either single heterozygote.

(Huang et al., 2007)

mew^M6, if^k27e double mutant dorsal branch terminal cell clones show a loss of terminal branches and an increase in lumen density and complexity in the remaining branches.

(Levi et al., 2006)

When tested in the odour-induced jump-test, double heterozygotes of sws^olfE-x26 and if^k27e exhibit a reduced response to benzaldehyde, but not to iso-amyl acetate or ethyl acetate, compared to controls.

(Ayyub and Paranjape, 2002)

In if^k27e/+ sli²/+ double heterozygous mutants the frequency of midline guidance errors is increased over the level observed in if^k27e homozygous mutants. 40% of segments had midline guidance defects of the innermost lateral axon tract (as assayed by Fas2). The frequency of midline crossing is much higher in if^k27e/Y;sli^unspecified mutants and also involves more lateral tracts.

(Stevens and Jacobs, 2002)

In combination with either mys^olfC-x3, mys^olfC-x5, mys^olfC-x10 or mys^olfC-x17, if^k27e flies show a reduced olfactory response to isoamyl acetate and benzaldehyde. In combination with mys^olfC-x3, mys^olfC-x5 or mys^olfC-x17 (but not mys^olfC-x10), if^k27e flies show a reduced olfactory response to ethyl acetate.

(Ayyub et al., 2000)

mew⁰²³ if^k27e or mew⁴⁹⁸ if^k27e double mutants have no midgut constrictions. Scer\GAL4^how-24B-mediated expression of if^{Δ.C.Scer\UAS} or if^{Δ.m8.Scer\UAS} rescues initiation of midgut constrictions.

(Li et al., 1998)

Double mutants for mew and if have a midgut phenotype as severe as that of mys mutants. Muscles detach, but later in development than in mys mutants. Dorsal hole and U-shaped cuticle of mys mutants are not observed in mew or if mutants. Double mutants between mew⁴⁹⁸, mew⁰²³ or mew^M6 and if^k27e or if^B4 do not show the twisted germband, amnioserosal detachment, dorsal movement of germband, dorsal hole and U-shaped embryo phenotypes of mys mutants, but do show early muscle detachments, as seen for mys mutants.

(Roote and Zusman, 1995)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Rescued by

if^k27e is rescued by Scer\GAL4^how-24B/if^C.UAS

(Li et al., 1998)

if^k27e is rescued by Scer\GAL4^how-24B/if^m8.UAS

(Li et al., 1998)

if^k27e is rescued by Scer\GAL4^how-24B/if^C.UAS

(Roote and Zusman, 1996)

if^k27e is rescued by Scer\GAL4^how-24B/if^m8.UAS

(Roote and Zusman, 1996)

if^k27e is rescued by if^+t39

(Brown, 1994)

Partially rescued by

if^k27e is partially rescued by Scer\GAL4^elav.PLu/if^C.UAS

(Hoang and Chiba, 1998)

if^k27e is partially rescued by if^Δ.C.UAS/Scer\GAL4^how-24B

(Li et al., 1998)

if^k27e is partially rescued by if^Δ.m8.UAS/Scer\GAL4^how-24B

(Li et al., 1998)

Comments

The nervous system phenotype is partially rescued by if^C.Scer\UAS expressed under the control of Scer\GAL4^elav.PLu.

(Hoang and Chiba, 1998)

Scer\GAL4^how-24B-mediated expression of if^{Δ.C.Scer\UAS} or if^{Δ.m8.Scer\UAS} only rescues the germband separation phenotype. Wing blisters from somatic clones can be rescued by Scer\GAL4^how-24B-mediated expression of either if^C.Scer\UAS or if^m8.Scer\UAS. Expression of if^{Δ.C.Scer\UAS} or if^{Δ.m8.Scer\UAS} does not rescue the blisters.

(Li et al., 1998)

The lethality caused by if^k27e can be rescued by Scer\GAL4^how-24B mediated expression of one copy of P{UAS-if.C}, a copy of both P{UAS-if.C} and P{UAS-if.m8} or two copies of either P{UAS-if.C} or P{UAS-if.m8}. Adult survivors carrying one copy of P{UAS-if.C} exhibit wing blisters at a higher frequency than the other survivors. Expression of one copy of P{UAS-if.m8} fails to rescue lethality, embryos die during development and fail to emerge from the egg cases. These embryos exhibit a muscle phenotype. Mitotic clones in the eye have normal morphology.

(Roote and Zusman, 1996)

Images (0)

Mutant

Wild-type

Stocks (2)

Bloomington

2177

g² if^k27e f^36a/FM7c

Kyoto

106686

g² if^k27e f^36a/FM7c

Notes on Origin

Discoverer

Comments

Class 0 mutation.

(Bloor and Brown, 1998)

No detectable PS2α protein.

(Wilcox et al., 1989)

Very little protein made by this allele.

(Brower, 1992)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (5)

Reported As

Symbol Synonym

if^K27E

(Ritzenthaler and Chiba, 2003, Hoang and Chiba, 1998)

if^K27e

(Li et al., 1998, Stark et al., 1997, Pankratz and Hoch, 1995)

if^k27E

(Huang et al., 2007)

if^k27e

(Ismat et al., 2013, Lin et al., 2013, Kim et al., 2012, Gilsohn and Volk, 2010, Popodi et al., 2010-, Chen et al., 2008, Tsai et al., 2008, Levi et al., 2006, Ayyub and Paranjape, 2002)

l(1)k27e

(Hoang and Chiba, 1998)

Name Synonyms

Secondary FlyBase IDs

FBal0092955

References (31)

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