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General Information
Symbol
Dmel\htlDN.UAS.cMb
Species
D. melanogaster
Name
FlyBase ID
FBal0090413
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
UAS-htlDN, UAS-DNhtl, htlDN
Key Links
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
Carried in construct
Cytology
Nature of the lesion
Statement
Reference

A truncated form of htl (truncated at amino acid residue Glu395) is expressed under the control of UAS regulatory sequences.

Allele components
Product class / Tool use(s)
Encoded product / tool
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

axon & mechanosensory neuron & adult head, with Scer\GAL4sca-537.4

axon & mechanosensory neuron & adult head, with Scer\GAL4sca-537.4, htlAB42

axon & ocellus sensory structure, with Scer\GAL4sca-537.4

axon & ocellus sensory structure, with Scer\GAL4sca-537.4, htlAB42

Detailed Description
Statement
Reference

Third instar larvae expressing htlDN.UAS.cMb under the control of Scer\GAL4repo.PU exhibit fewer glial nuclei along peripheral nerves, where no bulges are observed, as compared to controls.

Expression of htlDN.Scer\UAS.cMb in retinal basal glial (RBG) cell clones under the control of Scer\GAL4repo results in a reduction in RBG cell number, loss of differentiation and lack of migration in third instar larvae.

Expression of htlDN.Scer\UAS.cMb in the longitudinal visceral muscle (LVM) founder cells under the control of Scer\GAL4tey-5053A results in a reduction in the number of founder cells and cell death close to the trunk visceral mesoderm (TVM). LVM founder cell migration is incomplete.

Expression of htlDN.Scer\UAS.cMb driven by Scer\GAL4how-24B significantly reduces the number of boutons per muscle at the neuromuscular junction of third instar larvae, compared to controls.

Evoked excitatory junction potential (EJP) and miniature EJP (mEJP) amplitude are significantly increased (there is no significant difference in quantal content or mEJP frequency) at the NMJ of Scer\GAL4how-24B>htlDN.Scer\UAS.cMb third instar larvae, compared to controls.

Expression of htlDN.Scer\UAS.cMb under the control of Scer\GAL4repo results in a reduction in glial cell number and impaired glial migration in the eye disc.

Expression of htlDN.Scer\UAS.cMb under the control of Scer\GAL41151 results in a decrease in the number of founder cells per hemisegment compared to wild-type hemisegments; in 49% of Scer\GAL41151>htlDN.Scer\UAS.cMb hemisegments there are ~4 founder cells instead of the wild-type range of 17-22 and in 17% of hemisegments dorsal founders are completely absent. The number of myoblasts is not affected.

Expression of htlDN.Scer\UAS.cMb under the control of Scer\GAL4fkh.PH does not cause defects in salivary gland shape or position.

Expression of htlDN.Scer\UAS.cMb under the control of Scer\GAL4dpp.blk1 has no effect on furrow formation in the eye disc.

Individuals expressing htlDN.Scer\UAS.cMb exhibit abnormal pathfinding behaviour in ocellar pioneer (OP) and bristle mechanosensory (BM) axons in a dose dependant manner. This phenotype is enhanced by the addition of htlAB42. The axon guidance and extension alterations seen in htlDN.Scer\UAS.cMb individuals can be sorted into five different types. In type a, before head eversion OP axons spread abnormally, after head eversion OP axons can be seen to follow the trajectory of the BM axons. The type b defect consists of OP axons that extend normally detached from the epithelium but are unable to cross to the brain at the normal choice point. Instead they continue extending along the head contour. This type of defect is sometimes seen when one copy of htlDN.Scer\UAS.cMb is driven by Scer\GAL4sca-537.4, it is seen in all cases when 2 copies are driven. After head eversion this alteration results in an OP nerve that projects away from the epoidermal surface inside the head and reaches an ectopic position (sometimes terminating in the fat tissue in front of the brain.) The type c phenotypic class includes the BM axons. These axons always initially extend in the correct orientation, but when reaching the appropriate choice point just dorsal to the antena, they fail to detach from the epidermis and fail to cross and project into the brain. INstead they turn on themselves or on other converging BM axons and project backwards. Remarkably, these BM axons can sometimes perforate the epithelium and project outside the head, in the space between the old pupal cuticle molt and the newly deposited adult cuticle. Less frequently BM axons can be observed stalling in the epidermis or extending abnormally separated from the epidermal surface.

There is an absence of muscle founder cells in embryos expressing htlDN.Scer\UAS.cMb under the control of Scer\GAL4twi.PB.

Embryos expressing htlDN.Scer\UAS.cMb under the control of both Scer\GAL4twi.PG and Scer\GAL4Mef2.PR show partial loss of cardial cells, pericardial cells and somatic muscles. Small gaps in the normally continuous rows of visceral mesoderm progenitors are also seen. These embryos show normal early mesoderm dorsolateral migration.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Enhanced by
Statement
Reference

Scer\GAL4sca-537.4, htlDN.UAS.cMb has axon & mechanosensory neuron & adult head phenotype, enhanceable by Egfr[+]/Egfrunspecified

NOT Enhanced by
Statement
Reference

Scer\GAL4sca-537.4, htlDN.UAS.cMb has axon & ocellus sensory structure phenotype, non-enhanceable by EgfrE3/Egfr[+]

Suppressed by
NOT suppressed by
Statement
Reference

Scer\GAL4sca-537.4, htlDN.UAS.cMb has axon & mechanosensory neuron & adult head phenotype, non-suppressible by EgfrE3/Egfr[+]

Suppressor of
Additional Comments
Genetic Interactions
Statement
Reference

The addition of EgfrE3 to EgfrDN.Scer\UAS.cBa animals (when driven by Scer\GAL4unspecified) causes a suppression of the Ocellar pioneer (OP) axon phenotypes and an enhancement of the bristle mechanosensory (BM) phenotypes.

The addition of Egfrunspecified to EgfrDN.Scer\UAS.cBa animals (when driven by Scer\GAL4unspecified) causes a suppression of the Ocellar pioneer (OP) axon phenotypes and an enhancement of the bristle mechanosensory (BM) phenotypes.

An intermediate number of muscle founder cells are produced when both htlDN.Scer\UAS.cMb and Ras85DG13Q.Scer\UAS are co-expressed under the control of Scer\GAL4twi.PB compared to when either htlDN.Scer\UAS.cMb or Ras85DG13Q.Scer\UAS alone is expressed under the control of Scer\GAL4twi.PB (no muscle founder cells or supernumerary muscle founder cells respectively).

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
Comments
Comments

The htl protein produced acts as a dominant negative.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
Reported As
Symbol Synonym
htlDN.Scer\UAS.cMb
htlDN.UAS.cMb
Name Synonyms
Secondary FlyBase IDs
    References (26)