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General Information
Symbol
Dmel\jing3
Species
D. melanogaster
Name
FlyBase ID
FBal0138216
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Allele class
Nature of the Allele
Allele class
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
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 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In

commissure & growth cone

Detailed Description
Statement
Reference

In control stage 15 embryos, the anterior and posterior lateral trunks (Lta and Ltp, respectively) from adjacent segments are joined. In contrast, gaps occur between the Lta and Ltp in stage 15 homozygous jing3 embryos.

By stage 15, in control embryos, tracheal ganglionic cells and branches enter the ventral nerve cord (VNC) toward the central nervous system (CNS) midline. In contrast, three ganglionic branch (Gb) phenotypes are observed in in jing3 homozygotes: (1) Gbs do not reach the CNS midline appearing truncated; (2) Gbs show breaks; and (3) Gbs are absent from ventral positions

In contrast to control stage 13 embryos, the dorsal branch (Db) in jing3 embryos appear truncated and there are breaks in the dorsal trunk (Dt) as well. In stage 15 homozygous jing3 embryos, there are Dt gaps and Db breaks, Dt constrictions and truncated Db. The aberrant tracheal patterning in association with jing3 does not appear to be caused by cell loss. An additional phenotype observed in jing3 mutant embryos is the aberrant presence of Db cells in adjacent tracheal metameres instead of near the dorsal midline as in control embryos.

Fas2-positive longitudinal axons aberrantly cross the central nervous system midline in stage 16 homozygous embryos.

robo-positive and Fas2-positive longitudinal axons cross the central nervous system midline in jing3/Df(2R)ST1 stage 16 embryos.

Longitudinal glia inappropriately occupy positions at the central nervous system midline in stage 12 jing3/Df(2R)ST1 embryos.

jing3/Df(2R)ST1 embryos have a normal number of glia in the ventral nerve cord at stage 12, but the number of glia is reduced compared to controls at stage 15.

37.8% of stage 14 homozygous embryos have a reduced number of midline glial cells. jing3/Df(2R)ST1 embryos have a reduced number of midline glial cells. The embryos have breaks in the dorsal trunk of the tracheal system at stage 15.

The initial formation of the circumesophageal connectives appears normal during stage 12 in homozygous embryos, as both descending and ascending axons meet and fasciculate to form a connective. However, the preoral commissure is not pioneered in stage 12/0 homozygous embryos and formation of the preoral commissure has still not occurred in stage 15 homozygous embryos. The postoral tritocerebral commissure and circumesophageal connectives are reduced compared to wild type in stage 15 homozygous embryos and the connection between the brain and the ventral nerve cord is absent. The number of apoptotic glia in stage 11 homozygous embryonic brains is not significantly altered compared to wild type. At stage 15, mutant brains contain an increased number of apoptotic glia and a reduction in the total number of glia in the brain compared to wild type. Stage 15 mutant embryos show an approximately 26% reduction in the number of cas-expressing neurons in the brain compared to wild type, while cell death of these neurons is increased in the mutant brains. The number of sim-positive cells in the brain is reduced by about 50% in stage 15 mutants compared to wild type.

In jing3 homozygous embryos, commissural growth cones are often in the midline by stage 12. By stage 14, mutants show losses of longitudinal connections and reduced commissures compared to wild-type. The longitudinal fascicles stall within segment boundaries causing breaks in the longitudinal tracts in 95% of mutants. A subset of normally ipsilateral axons of the most medial fascicle project instead contralaterally, suggesting that midline repulsive mechanisms are perturbed. In wild-type embryos, one or two apoptotic glia are seen within the entire nerve cord of a stage 12 embryo. By contrast, every nerve cord segment in jing3 mutant embryos contains apoptotic glia. Loss of VUMs, MNB MP1, vMP2 and dMP2 neurons are seen. Ectodermal segmentation appears relatively normal in mutants. Compared to about three in wild-type embryos, about 20 apoptotic cells are seen in stage 11 mutant embryos. There is also an increase in the number of apoptotic profiles surrounding the tracheal pits in mutants. Cell death is observed throughout embryogenesis in all tracheal branches in mutants. Homozygotes exhibit tracheal defects; tracheal cells invaginate but the tracheal branches do not migrate properly anteriorly across en-positive stripes. By stage 15, parts of the dorsal trunk, the dorsal branch and transverse connectives are missing and correlate with a loss of cells by apoptosis. In addition the visceral branch does not form in mutants. The overall embryonic pattern of cell death is similar to wild-type, suggesting the CNS and tracheal phenotypes are specific to those systems.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
NOT Enhanced by
Statement
Reference

jing3 has visceral branch phenotype, non-enhanceable by trh1

jing3 has dorsal trunk primordium phenotype, non-enhanceable by trh1

Suppressed by
NOT suppressed by
Statement
Reference

jing3 has visceral branch phenotype, non-suppressible by trh1

jing3 has dorsal trunk primordium phenotype, non-suppressible by trh1

NOT Enhancer of
Statement
Reference
NOT Suppressor of
Statement
Reference
Other
Additional Comments
Genetic Interactions
Statement
Reference

In contrast to single heterozygous vvldfr-E82 or jing3 mutants, double heterozygous embryos show tracheal ganglionic branch defects.

In contrast to single heterozygous pntΔ88 or jing3 mutants, double heterozygous embryos show tracheal ganglionic branch defects.

jing3/vvldfr-E82 double heterozygotes show significant losses in the continuity of tracheal tubules (gaps and breaks) and constrictions in the dorsal trunk (Dt), similar to the homozygous phenotypes of jing3 and less severe than that of homozygous vvldfr-E82.

jing3/pntΔ88 double heterozygotes show significant losses in the continuity of tracheal tubules (gaps and breaks) and constrictions in the dorsal trunk (Dt), similar to the homozygous phenotypes of jing3 and less severe than that of homozygous vvldfr-E82.

jing3/pntE039 double heterozygotes show significant losses in the continuity of tracheal tubules (gaps and breaks) and constrictions in the dorsal trunk (Dt), similar to the homozygous phenotypes of jing3 and less severe than that of homozygous vvldfr-E82.

Dorsal branches are absent, truncated or broken in jing3/pntΔ88 double heterozygotes.

Dorsal branches are absent, truncated or broken in jing3/pntΔ88 double heterozygotes.

Expression of Ras85DV12.Scer\UAS under the control of Scer\GAL4sim.P3.7 reduces the penetrance of the loss of midline glia phenotype seen in homozygous jing3 embryos, so that only 11.3% of double mutant embryos have a reduced number of midline glial cells. Expression of EgfrElp.Scer\UAS under the control of Scer\GAL4sim.P3.7 reduces the penetrance of the loss of midline glia phenotype seen in homozygous jing3 embryos, so that only 20% of double mutant embryos have a reduced number of midline glial cells. Expression of EgfrElp.Scer\UAS under the control of Scer\GAL4sim.P3.7 reduces the penetrance of the loss of midline glia phenotype seen in jing3/Df(2R)ST1 embryos. jing3/spi1 double heterozygous embryos have an increased number of apoptotic cells in the CNS midline at stage 12 compared to wild type (where cell death is uncommon at this stage). SIIN/jing3 and jing3/spi1 double heterozygous embryos have breaks in the dorsal trunk of the tracheal system at stage 15.

The addition of jing3 to sim2 has no effect on the sim2 collapsed axon phenotype. The addition of trh1 to jing3 homozygotes has no effect on the jing3 tracheal phenotype.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
Comments
Comments

Phenotypic analysis suggests the following allelic series: jing3 > jing2 > jing1.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (1)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (5)