FlyBase Allele Report: Dmel\JIL-1[z2]

General Information

Symbol

Dmel\JIL-1^z2

Species

D. melanogaster

Name

FlyBase ID

FBal0122076

Feature type

allele

Associated gene

Dmel\JIL-1

Associated Insertion(s)

P{5'EP}JIL-1^z2

Carried in Construct

Key Links

Allele class

loss of function allele

Mutagen

Delta2-3 transposase

Nature of the Allele

Allele class

loss of function allele

(Lerach et al., 2006, Zhang et al., 2006)

Mutagen

Delta2-3 transposase

(Wang et al., 2001)

Progenitor genotype

JIL-1^EP3657

(Wang et al., 2001)

Associated Insertion(s)

P{5'EP}JIL-1^z2

Cytology

Description

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.

(Zhang et al., 2003)

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.

(Wang et al., 2001)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

Variant Molecular Consequences

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

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

abnormal mitotic cell cycle | third instar larval stage

(Ding et al., 2009)

enhancer of variegation (with JIL-1^z60), with P{hsp26-pt-T}39C-3

(Bao et al., 2007)

enhancer of variegation (with JIL-1^z60), with P{hsp26-pt-T}118E-10

(Bao et al., 2007)

enhancer of variegation (with JIL-1^z60), with P{hsp26-pt-T}118E-25

(Bao et al., 2007)

enhancer of variegation (with JIL-1^z60), with P{hsp26-pt-T}118E-32

(Bao et al., 2007)

female sterile (with JIL-1^h9)

(Zhang et al., 2003)

lethal (with JIL-1^z60)

(Zhang et al., 2006)

lethal | recessive

(Deng et al., 2007, Zhang et al., 2003, Wang et al., 2001, Wang et al., 2001)

lethal - all die during embryonic stage | maternal effect (with JIL-1^EP3657)

(Zhang et al., 2003)

lethal - all die during embryonic stage | maternal effect (with JIL-1^h9)

(Zhang et al., 2003)

lethal - all die during embryonic stage | maternal effect | partially (with JIL-1^Scim)

(Zhang et al., 2003)

lethal - all die during embryonic stage | maternal effect | partially (with JIL-1^z28)

(Zhang et al., 2003)

partially lethal - majority die (with JIL-1^z60)

(Bao et al., 2007, Lerach et al., 2006)

some die during embryonic stage | maternal effect (with JIL-1^EP3657)

(Zhang et al., 2003)

some die during embryonic stage | maternal effect (with JIL-1^h9)

(Zhang et al., 2003)

some die during embryonic stage | partially (with JIL-1^Scim)

(Zhang et al., 2003)

some die during embryonic stage | partially (with JIL-1^z28)

(Zhang et al., 2003)

suppressor of variegation (with JIL-1^h9), with In(1)w^m4

(Lerach et al., 2006)

suppressor of variegation (with JIL-1^z60), with In(1)w^m4

(Lerach et al., 2006)

visible | homeotic (with JIL-1^EP3657)

(Zhang et al., 2003)

Phenotype Manifest In

abdominal sternite 5 | ectopic | male (with JIL-1^EP3657)

(Zhang et al., 2003)

abdominal sternite 6 | male (with JIL-1^EP3657)

(Zhang et al., 2003)

egg (with JIL-1^h9)

(Zhang et al., 2003)

egg chamber (with JIL-1^h9)

(Zhang et al., 2003)

euchromatin

(Wang et al., 2001)

larval neuroblast | third instar larval stage

(Ding et al., 2009)

nurse cell (with JIL-1^h9)

(Zhang et al., 2003)

oocyte nucleus (with JIL-1^h9)

(Zhang et al., 2003)

ovariole (with JIL-1^h9)

(Zhang et al., 2003)

ovary (with JIL-1^h9)

(Zhang et al., 2003)

polytene chromosome

(Deng et al., 2007, Zhang et al., 2006, Zhang et al., 2003, Wang et al., 2001)

polytene chromosome (with JIL-1^h9)

(Zhang et al., 2006, Zhang et al., 2003)

polytene chromosome | larval stage

(Bao et al., 2008)

polytene chromosome | male

(Wang et al., 2001)

polytene chromosome band | male

(Zhang et al., 2006)

polytene chromosome band | male (with JIL-1^h9)

(Zhang et al., 2006)

polytene chromosome interband

(Wang et al., 2001)

polytene chromosome interband (with JIL-1^h9)

(Zhang et al., 2003)

spindle | third instar larval stage

(Ding et al., 2009)

Detailed Description

Statement

Reference

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

(Li et al., 2017)

Expression of JIL-1^{Scer\UAS.T:Avic\GFP-ECFP} in a JIL-1^z2; w^118E-10/+ mutant background, under the control of Scer\GAL4^da.G32, leads to a variegated eye phenotype.

Expression of JIL-1^{CTD.Scer\UAS.T:Avic\GFP-ECFP} in a JIL-1^z2; w^118E-10/+ mutant background, under the control of Scer\GAL4^da.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-1^{ΔCTD.Scer\UAS.T:Avic\GFP-ECFP} in a JIL-1^z2; w^118E-10/+ mutant background, under the control of Scer\GAL4^da.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.

(Wang et al., 2011)

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

(Ding et al., 2009)

JIL-1^z2 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.

(Bao et al., 2008)

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.

(Deng et al., 2007)

In JIL-1^z2 and JIL-1^z2/JIL-1^h9 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-1^z2/JIL-1^z60 flies eclose.

(Zhang et al., 2006)

Only 8% of embryos derived from JIL-1^z2/JIL-1^EP3657 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-1^z2/JIL-1^EP3657

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

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

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

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

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

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

adults is about half that of comparable sibling classes.

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

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

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

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

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

animals that pupariate survive to adult eclosion.

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

wild-type males hatch.

41% of embryos derived from JIL-1^z2/JIL-1^z28 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-1^z2/JIL-1^Scim 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-1^z2/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-1^z2/JIL-1^z2

larval polytene chromosomes have a very similar phenotype, although

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

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

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

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-1^z2/JIL-1^EP3657 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-1^z2 allele is maternally or paternally derived).

(Zhang et al., 2003)

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.

(Wang et al., 2001)

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.

(Wang et al., 2001)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressed by

Statement

Reference

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

(Deng et al., 2007)

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

(Deng et al., 2007)

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

(Deng et al., 2007)

JIL-1^z2 has lethal | recessive phenotype, suppressible by Su(var)3-9¹/Su(var)3-9²

(Deng et al., 2007)

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

(Zhang et al., 2006)

NOT suppressed by

Statement

Reference

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

(Deng et al., 2007)

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

(Deng et al., 2007)

Enhancer of

Statement

Reference

JIL-1^z2 is an enhancer of lethal | third instar larval stage phenotype of Chro⁷¹/Chro⁶¹²

(Rath et al., 2006)

JIL-1[+]/JIL-1^z2 is an enhancer of visible | dominant | homeotic phenotype of brm[+]/brm², trx^E2

(Zhang et al., 2003)

NOT Enhancer of

Statement

Reference

JIL-1[+]/JIL-1^z2 is a non-enhancer of partially lethal | male phenotype of Df(1)52, P{w⁺4Δ4.3}, lncRNA:roX1^ex6, lncRNA:roX1^t4.9

(Prabhakaran and Kelley, 2012)

Suppressor of

Statement

Reference

JIL-1^z2/JIL-1^h9 is a suppressor | partially of enhancer of variegation | dominant phenotype of E(var)2-1¹, In(1)w^m4

(Lerach et al., 2006)

NOT Suppressor of

Statement

Reference

JIL-1[+]/JIL-1^z2 is a non-suppressor of partially lethal | male phenotype of Df(1)52, P{w⁺4Δ4.3}, lncRNA:roX1^ex6, lncRNA:roX1^t4.9

(Prabhakaran and Kelley, 2012)

JIL-1^z2 is a non-suppressor of lethal phenotype of Su(var)205⁵/Su(var)205⁴

(Deng et al., 2007)

Phenotype Manifest In

Suppressed by

Statement

Reference

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

(Deng et al., 2007)

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

(Deng et al., 2007)

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

(Deng et al., 2007)

JIL-1^z2 has polytene chromosome phenotype, suppressible by Su(var)3-9¹/Su(var)3-9²

(Deng et al., 2007)

NOT suppressed by

Statement

Reference

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

(Deng et al., 2007)

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

(Deng et al., 2007)

JIL-1^z2 has polytene chromosome phenotype, non-suppressible by Su(var)205⁵/Su(var)205⁴

(Deng et al., 2007)

Enhancer of

Statement

Reference

JIL-1[+]/JIL-1^z2 is an enhancer of adult abdominal segment 5 | ectopic | male phenotype of brm[+]/brm², trx^E2

(Zhang et al., 2003)

JIL-1[+]/JIL-1^z2 is an enhancer of adult abdominal segment 6 | male phenotype of brm[+]/brm², trx^E2

(Zhang et al., 2003)

NOT Suppressor of

Statement

Reference

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

(Deng et al., 2007)

Additional Comments

Genetic Interactions

Statement

Reference

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

The abnormal polytene chromosome morphology seen in JIL-1^z2 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-1^z2.

The defects in polytene chromosome morphology seen in JIL-1^z2 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-1^z2/JIL-1^z2 double mutants resembles that of JIL-1^z2/JIL-1^z2 single mutants.

(Deng et al., 2007)

JIL-1^z2/JIL-1^z60 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.

(Zhang et al., 2006)

The frequency of A6 to A5 transformation seen in brm² trx^E2 double heterozygous males is increased if they also carry JIL-1^z2; the frequency is 65% if JIL-1^z2 is maternally derived and brm² trx^E2 is paternally derived and is 75% in the reciprocal cross.

(Zhang et al., 2003)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Rescued by

JIL-1^z2 is rescued by JIL-1^Hsp83.GFP

(Bao et al., 2008)

JIL-1^z2 is rescued by JIL-1^UAS.Tag:V5/Scer\GAL4^hs.PB

(Bao et al., 2008)

JIL-1^z2 is rescued by JIL-1^{CTD.UAS.ECFP,Tag:NLS(SV40-largeT)}/Scer\GAL4^hs.PB

(Bao et al., 2008)

JIL-1^z2 is rescued by JIL-1^Hsp83.GFP

(Wang et al., 2001)

Partially rescued by

JIL-1^z2 is partially rescued by JIL-1^{UAS.lacI(DBD)}

(Li et al., 2013)

JIL-1^z2 is partially rescued by JIL-1^{ΔCTD.UAS.lacI(DBD)}

(Li et al., 2013)

JIL-1^z2 is partially rescued by JIL-1^{ΔNTD.UAS.lacI(DBD)}

(Li et al., 2013)

JIL-1^z2 is partially rescued by JIL-1^{CTD.UAS.lacI(DBD)}

(Li et al., 2013)

JIL-1^z2 is partially rescued by JIL-1^{KDImut.UAS.Tag:V5}

(Li et al., 2013)

JIL-1^z2 is partially rescued by JIL-1^{KDIImut.UAS.Tag:V5}

(Li et al., 2013)

JIL-1^z2 is partially rescued by JIL-1^{KDI-KDIImut.UAS.Tag:V5}

(Li et al., 2013)

JIL-1^z2 is partially rescued by JIL-1^{S424A.UAS.Tag:HA,Tag:FLAG}

(Li et al., 2013)

JIL-1^z2 is partially rescued by JIL-1^{KDI-KDII.UAS.Tag:V5,Tag:NLS(SV40-largeT)}/Scer\GAL4^hs.PB

(Bao et al., 2008)

JIL-1^z2 is partially rescued by JIL-1^{NTD-CTD.UAS.Tag:V5}/Scer\GAL4^hs.PB

(Bao et al., 2008)

JIL-1^z2 is partially rescued by JIL-1^{ΔCTD.UAS.GFP}/Scer\GAL4^hs.PB

(Bao et al., 2008)

Not rescued by

JIL-1^z2 is not rescued by JIL-1^{NTD.UAS.Tag:V5}/Scer\GAL4^hs.PB

(Bao et al., 2008)

Comments

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

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

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

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

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

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

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

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

(Li et al., 2013)

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

Expression of JIL-1^{Scer\UAS.T:SV5\V5} under the control of the Scer\GAL4^hs.PB driver rescues both the autosomal and male X polytene chromosome phenotypes seen in JIL-1^z2 homozygous larvae. The Scer\GAL4^hs.PB driver is leaky and therefore no heat shock is required.

Expression of JIL-1^{NTD.Scer\UAS.T:SV5\V5} under the control of the Scer\GAL4^hs.PB driver fails to rescue either the autosomal or the male X polytene chromosome phenotypes seen in JIL-1^z2 homozygous larvae. The Scer\GAL4^hs.PB driver is leaky and therefore no heat shock is required.

Expression of JIL-1^{KDI-KDII.Scer\UAS.T:SV5\V5,T:SV40\nls2} under the control of the Scer\GAL4^hs.PB driver partially rescues the uncoiling and loss of banding phenotypes seen in the autosomal polytene chromosomes of JIL-1^z2 homozygous larvae. The phenotypes seen in the male X chromosome are not rescued. The Scer\GAL4^hs.PB driver is leaky and therefore no heat shock is required.

Expression of JIL-1^{NTD-CTD.Scer\UAS.T:SV5\V5} under the control of the Scer\GAL4^hs.PB driver partially rescues both the autosomal and male X polytene chromosome phenotypes seen in JIL-1^z2 homozygous larvae. The Scer\GAL4^hs.PB driver is leaky and therefore no heat shock is required.

Expression of JIL-1^{CTD.Scer\UAS.T:Avic\GFP-ECFP,T:SV40\nls2} under the control of the Scer\GAL4^hs.PB driver rescues both the autosomal and male X polytene chromosome phenotypes seen in JIL-1^z2 homozygous larvae. The Scer\GAL4^hs.PB driver is leaky and therefore no heat shock is required.

Expression of JIL-1^{ΔCTD.Scer\UAS.T:Avic\GFP} under the control of the Scer\GAL4^hs.PB driver rescues the autosomal polytene chromosome phenotypes seen in JIL-1^z2 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\GAL4^hs.PB driver is leaky and therefore no heat shock is required.

(Bao et al., 2008)

Images (0)

Mutant

Wild-type

Stocks (1)

Bloomington

93142

y¹ w^*; P{5'EP}JIL-1^z2/TM6C, Sb¹ Tb¹

Notes on Origin

Discoverer

Comments

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

(Zhang et al., 2003)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (3)

Reported As

Symbol Synonym

JIL-1^Z2

JIL-1^z2

(Albig et al., 2019, Girton et al., 2013, Li et al., 2013, Wang et al., 2011, Ding et al., 2009, Bao et al., 2008, Cai et al., 2008, Bao et al., 2007, Deng et al., 2007, Ivaldi et al., 2007, Lerach et al., 2006, Rath et al., 2006)

Jil-1^Z2

(Li et al., 2017, Prabhakaran and Kelley, 2012)

Name Synonyms

Secondary FlyBase IDs

References (19)

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