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General Information
Symbol
Dmel\JIL-1z2
Species
D. melanogaster
Name
FlyBase ID
FBal0122076
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Imprecise excision resulting in a deletion removing nucleotides 204,172 to sequences within the region between nucleotides 198,609 to 197,546 of genomic scaffold AE003546 (release 3.0, GI:23093654 ). This removes the start codon along with sequences extending into the second intron and deletes the P{EP} element's promoter sequences.

Imprecise excision of the P{EP} element (the 3' end has been excised), removing JIL-1 sequence from the P{EP} insertion site through most of intron II, which removes the start codon region.

Insertion components
P{5'EP}JIL-1z2
Expression Data
Reporter Expression
Additional Information
Statement
Reference
 
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 0 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

JIL-1z2 mutant larvae do not display any central neuroblast reactivation defects.

Expression of JIL-1Scer\UAS.T:Avic\GFP-ECFP in a JIL-1z2; w118E-10/+ mutant background, under the control of Scer\GAL4da.G32, leads to a variegated eye phenotype.

Expression of JIL-1CTD.Scer\UAS.T:Avic\GFP-ECFP in a JIL-1z2; w118E-10/+ mutant background, under the control of Scer\GAL4da.G32, enhances the position effect variegation seen in the eye, as indicated by a decrease in the proportion of red ommatidia and a statistically significant 54% decrease in optical density of eye pigment levels.

Expression of JIL-1ΔCTD.Scer\UAS.T:Avic\GFP-ECFP in a JIL-1z2; w118E-10/+ mutant background, under the control of Scer\GAL4da.G32, suppresses the position effect variegation seen in the eye, as indicated by an increases in the proportion of red ommatidia and a statistically significant 151% increase in the optical density of eye pigment levels.

A small number of JIL-1z2 mutant neuroblasts show disrupted spindle morphology (18%) compared to wildtype (8%).

JIL-1z2 homozygous mutants exhibit phenotypes in larval polytene chromosomes. Phenotypes include autosomal uncoiling, puffing of the male X chromosome and loss of discrete band/interband regions.

Homozygous third instar larvae show defects in polytene chromosome morphology; there is misalignment and intermixing of interband and banded regions and extensive coiling and folding of the chromosome arms. The male X chromosome is particularly affected and no remnants of banded regions are discernible.

In JIL-1z2 and JIL-1z2/JIL-1h9 mutants the morphology of the polytene chromosomes is perturbed with coiled and compacted chromosome arms. The male X polytene chromosome shows the most extreme version of this phenotype with no coherent bands visible. Only 1 out of 871 JIL-1z2/JIL-1z60 flies eclose.

Only 8% of embryos derived from JIL-1z2/JIL-1EP3657 females mated to wild-type males hatch, of those larvae that hatch, 58% survive

to pupation, and of those that survive to pupation 95% eclose.

94% of embryos derived from wild-type females mated to JIL-1z2/JIL-1EP3657

males hatch, and of those larvae that hatch, 95% survive to pupation.

87% of embryos derived from JIL-1z2/+ females mated to JIL-1z2/JIL-1EP3657

males hatch, suggesting that some embryos with the JIL-1z2/JIL-1z2

or JIL-1z2/JIL-1EP3657 genotype can survive embryogenesis if

provided with normal maternal JIL-1 product. No JIL-1z2/JIL-1z2

progeny survive to eclosion and the number of surviving JIL-1z2/JIL-1EP3657

adults is about half that of comparable sibling classes.

71% of embryos derived from JIL-1z2/+ females mated to JIL-1z2/+

males hatch. Less JIL-1z2/JIL-1z2 larval progeny pupariate

than expected, suggesting that a significant fraction of the JIL-1z2/JIL-1z2

progeny die during the larval period. None of the JIL-1z2/JIL-1z2

animals that pupariate survive to adult eclosion, whereas 96% of JIL-1z2/+

animals that pupariate survive to adult eclosion.

0% of embryos derived from JIL-1z2/JIL-1h9 females mated to

wild-type males hatch.

41% of embryos derived from JIL-1z2/JIL-1z28 females mated

to wild-type males hatch, of those larvae that hatch, 71% survive to

pupation, and of those that survive to pupation 94% eclose.

60% of embryos derived from JIL-1z2/JIL-1Scim females mated

to wild-type males hatch, of those larvae that hatch, 80% survive to

pupation, and of those that survive to pupation 94% eclose.

JIL-1z2/Df(3L)h9 larval polytene chromosomes are abnormal; the

autosomes appear highly coiled and compact and the interband regions

are lost. In males, the X chromosome is even shorter and has a "puffy"

morphology. This phenotype is highly penetrant. JIL-1z2/JIL-1z2

larval polytene chromosomes have a very similar phenotype, although

the "puffing" of the X chromosome in males tends to be more extreme.

JIL-1z2/JIL-1h9 animals that survive to adulthood are sterile

and females produce significantly fewer eggs than normal. JIL-1z2/JIL-1h9

ovaries are significantly decreased in size compared to wild type,

consisting primarily of connective tissue with little or no apparent

ovariole development, although in some cases ovary tissue develops

to some degree. In those females with some ovary development, a range

of egg chamber defects are seen. The most common consists of egg chambers

with a reduction in the number of nurse cells and no apparent oocyte

nucleus. In other cases cell nuclei within the egg chamber appear

to fragment of fail to undergo DNA amplification. In a few cases,

egg chambers containing an increased number of nurse cells are seen.

In all cases, other ovarioles in the same ovary often appear empty

with no egg chamber development.

93% of JIL-1z2/JIL-1EP3657 males have ventral sternite bristles

on the A6 sternite, indicating a transformation of A6 to the more anterior

A5 segment.

Only 2% of heterozygous males show an A6 to A5 transformation (regardless

of whether the JIL-1z2 allele is maternally or paternally derived).

Lethality is 100%. Striking disorganization of larval polytene chromosomes with the most severe effect observed on the male X chromosome, resulting in its being significantly shorter and broader with a poorly defined to non-existent Hoechst banding pattern.

The polytene chromosome banding pattern is perturbed in homozygous third instar larvae; the euchromatin interband regions are largely absent and the chromosome arms are highly condensed. Perturbation of the male X chromosome is relatively more severe than that of the autosomes.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
Statement
Reference

JIL-1z2 has lethal | recessive phenotype, suppressible | partially by Su(var)3-9[+]/Su(var)3-96

JIL-1z2 has lethal | recessive phenotype, suppressible | partially by Su(var)3-91/Su(var)3-9[+]

JIL-1z2 has lethal | recessive phenotype, suppressible | partially by Su(var)3-9[+]/Su(var)3-92

JIL-1z60/JIL-1z2 has lethal phenotype, suppressible | partially by Su(var)3-91/Su(var)3-9[+]

NOT suppressed by
Statement
Reference

JIL-1z2 has lethal | recessive phenotype, non-suppressible by Su(var)205[+]/Su(var)2054

JIL-1z2 has lethal | recessive phenotype, non-suppressible by Su(var)2055/Su(var)205[+]

Enhancer of
Statement
Reference

JIL-1[+]/JIL-1z2 is an enhancer of visible | dominant | homeotic phenotype of brm[+]/brm2, trxE2

NOT Enhancer of
Statement
Reference
Suppressor of
Statement
Reference
NOT Suppressor of
Statement
Reference
Phenotype Manifest In
Suppressed by
Statement
Reference

JIL-1z2 has polytene chromosome phenotype, suppressible | partially by Su(var)3-91/Su(var)3-9[+]

JIL-1z2 has polytene chromosome phenotype, suppressible | partially by Su(var)3-9[+]/Su(var)3-92

JIL-1z2 has polytene chromosome phenotype, suppressible | partially by Su(var)3-9[+]/Su(var)3-96

NOT suppressed by
Statement
Reference

JIL-1z2 has polytene chromosome phenotype, non-suppressible by Su(var)205[+]/Su(var)2054

JIL-1z2 has polytene chromosome phenotype, non-suppressible by Su(var)2055/Su(var)205[+]

Enhancer of
Statement
Reference

JIL-1[+]/JIL-1z2 is an enhancer of adult abdominal segment 5 | ectopic | male phenotype of brm[+]/brm2, trxE2

JIL-1[+]/JIL-1z2 is an enhancer of adult abdominal segment 6 | male phenotype of brm[+]/brm2, trxE2

NOT Suppressor of
Statement
Reference

JIL-1[+]/JIL-1z2 is a non-suppressor of polytene chromosome phenotype of Su(var)2055/Su(var)2054

Additional Comments
Genetic Interactions
Statement
Reference

The lethality of JIL-1z2 homozygotes is significantly suppressed by one copy of Su(var)3-91 (87.4% viability), Su(var)3-92 (50.7% viability) or Su(var)3-96 (60.7% viability).

The lethality of JIL-1z2 homozygotes is significantly suppressed by Su(var)3-91/Su(var)3-92 (55.8% viability).

The abnormal polytene chromosome morphology seen in JIL-1z2 homozygous third instar larvae is partially suppressed by Su(var)3-91/+, Su(var)3-92/+, Su(var)3-96/+, Su(var)3-91/Su(var)3-92 or Su(var)3-96/Su(var)3-96; the chromosome arms ar to a large extent unfolded with reduced ectopic contacts and there is a clearly discernible banding pattern that in some cases almost resembles the wild-type pattern. However, there is no discernible improvement in the morphology of the male X chromosome in the double mutants.

The defects in polytene chromosome morphology seen in Su(var)2054/Su(var)2055 larvae are not altered by one copy of JIL-1z2.

The defects in polytene chromosome morphology seen in JIL-1z2 homozygous larvae are not altered by one copy of Su(var)2054 or Su(var)2055.

The polytene chromosome morphology of Su(var)2054/Su(var)2055 ; JIL-1z2/JIL-1z2 double mutants resembles that of JIL-1z2/JIL-1z2 single mutants.

JIL-1z2/JIL-1z60 flies that have one copy of the Su(var)3-91 allele show greater levels of survival compared to those that carry two wild-type copies of Su(var)3-9.

The frequency of A6 to A5 transformation seen in brm2 trxE2 double heterozygous males is increased if they also carry JIL-1z2; the frequency is 65% if JIL-1z2 is maternally derived and brm2 trxE2 is paternally derived and is 75% in the reciprocal cross.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments

JIL-1Scer\UAS.T:Ecol\lacI rescues polytene chromosome morphology in JIL-1z2 mutant animals. Rescue of adult viability is 58.6%.

JIL-1ΔCTD.Scer\UAS.T:Ecol\lacI rescues autosome polytene chromosome morphology in JIL-1z2 mutant animals, but the morphology of the male X chromosome is only partially rescued. Rescue of adult viability is only 4.4%.

JIL-1ΔNTD.Scer\UAS.T:Ecol\lacI restores polytene chromosome morphology in JIL-1z2 mutant animals to or near wild type. Rescue of adult viability is 18.9%.

JIL-1CTD.Scer\UAS.T:Ecol\lacI largely restores polytene chromosome morphology in JIL-1z2 mutant animals, including that of the male X chromosome. Rescue of adult viability is 13.6%.

JIL-1KDImut.Scer\UAS.T:SV5\V5 fails to rescue polytene chromosome morphology in JIL-1z2 mutant animals. Rescue of adult viability is 14.3%.

JIL-1KDIImut.Scer\UAS.T:SV5\V5 fails to rescue polytene chromosome morphology in JIL-1z2 mutant animals. Rescue of adult viability is 12.3%.

JIL-1KDI-KDIImut.Scer\UAS.T:SV5\V5 fails to rescue polytene chromosome morphology in JIL-1z2 mutant animals. Rescue of adult viability is 22.9%.

JIL-1S424A.Scer\UAS.T:Ivir\HA1,T:Zzzz\FLAG partially rescues autosome polytene chromosome morphology in JIL-1z2 mutant animals. Rescue of adult viability is 14.7%.

Expression of JIL-1Hsp83.T:Avic\GFP rescues both the autosomal and male X polytene chromosome phenotypes seen in JIL-1z2 homozygous larvae. The Hsp83 driver is leaky and therefore no heat shock is required.

Expression of JIL-1Scer\UAS.T:SV5\V5 under the control of the Scer\GAL4hs.PB driver rescues both the autosomal and male X polytene chromosome phenotypes seen in JIL-1z2 homozygous larvae. The Scer\GAL4hs.PB driver is leaky and therefore no heat shock is required.

Expression of JIL-1NTD.Scer\UAS.T:SV5\V5 under the control of the Scer\GAL4hs.PB driver fails to rescue either the autosomal or the male X polytene chromosome phenotypes seen in JIL-1z2 homozygous larvae. The Scer\GAL4hs.PB driver is leaky and therefore no heat shock is required.

Expression of JIL-1KDI-KDII.Scer\UAS.T:SV5\V5,T:SV40\nls2 under the control of the Scer\GAL4hs.PB driver partially rescues the uncoiling and loss of banding phenotypes seen in the autosomal polytene chromosomes of JIL-1z2 homozygous larvae. The phenotypes seen in the male X chromosome are not rescued. The Scer\GAL4hs.PB driver is leaky and therefore no heat shock is required.

Expression of JIL-1NTD-CTD.Scer\UAS.T:SV5\V5 under the control of the Scer\GAL4hs.PB driver partially rescues both the autosomal and male X polytene chromosome phenotypes seen in JIL-1z2 homozygous larvae. The Scer\GAL4hs.PB driver is leaky and therefore no heat shock is required.

Expression of JIL-1CTD.Scer\UAS.T:Avic\GFP-ECFP,T:SV40\nls2 under the control of the Scer\GAL4hs.PB driver rescues both the autosomal and male X polytene chromosome phenotypes seen in JIL-1z2 homozygous larvae. The Scer\GAL4hs.PB driver is leaky and therefore no heat shock is required.

Expression of JIL-1ΔCTD.Scer\UAS.T:Avic\GFP under the control of the Scer\GAL4hs.PB driver rescues the autosomal polytene chromosome phenotypes seen in JIL-1z2 homozygous larvae, with improved spread and more well resolved banding pattern than in wild type. The phenotypes seen in the male X chromosome are only partially rescued, with remnants of puffed regions still present. The Scer\GAL4hs.PB driver is leaky and therefore no heat shock is required.

Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
Comments
Comments

General trend from least to most viable is: JIL-1z2 < JIL-1h9 < JIL-1z60 < JIL-1EP3657 < JIL-1z28 ~ JIL-1Scim.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
References (19)