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General Information
Symbol
Dmel\tlll49
Species
D. melanogaster
Name
FlyBase ID
FBal0016893
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
tll149, tll49
Key Links
Allele class
Mutagen
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Nucleotide change:

T30852901A

Reported nucleotide change:

T596A

Amino acid change:

C78term | tll-PA

Reported amino acid change:

C78term

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Nucleotide substitution: T?A.

Mutation results in a protein that terminates in the second zinc finger at the Leu just before the second Cys.

Amino acid replacement: C78term.

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

tlll49 mutant embryos have significantly reduced proliferation of neuroblasts and daughters and significantly reduced numbers of neuroblasts, including type II neuroblasts, in the brain, compared to controls.

MARCM clones of tlll49 in the third instar mushroom body (MB) show a reduction in the number of labelled neurons to 8.7, compared to 200 in controls. In adults, this number barely increases (10.4, compared to >500 in controls), and the axonal projections of these mutant clones are predominantly restricted to the gamma lobes, but a few enter the alpha-prime and beta-prime lobes.

tlll49 mutant MB clones are not accompanied by identifiable neuroblasts at 40 hours after puparium formation (APF), whilst controls are associated with three or four even at 60 hours APF. There is a marked reduction in the incorporation of BrdU in tlll49 mutant MB clones at both the larval and pupal stages compared to controls, and most of the BrdU labelling is lost after a thirty two hour pulse-chase. Cell death is markedly increased in third instar larval ganglion mother cells in tlll49 MB clones compared to controls.

Single cell class IV dendrite arborisation (da) neuron clones that are homozygous for tlll49 do not show defects in the establishment or maintenance of dendritic tiling.

Mutant embryos lack the Fas2-positive protocerebral neuropile. ey-positive mushroom body cells seen in the dorsal protocerebrum of wild-type embryos are also missing in the mutant embryos.

Mutant embryos ar unable to hatch, but stay alive for up to 24 hours under oil.

Late stage mutant embryos move incessantly (wild-type embryos from stage 17d onwards show phases of movement that alternate with phases of complete stillness). The movement pattern of the mutant embryos can be best described as an uncoordinated contraction of individual segments. Segments at different positions along the antero-posterior axis frequently contract at the same time. Left and right hemisegments are often out of phase, and the mutant embryos undergo a high frequency "wiggling" motion. Peristaltic waves are all but absent in the mutant embryos.

tlll49 mutant stage 12 embyro dorsal head exhibit removal of most of the protocerebrum, including the pars intercerebralis.

The brain is strongly reduced in mutant stage 16 embryos, the stomatogastric nervous system is intact and the corpus cardiacum is absent.

The optic lobe placode appears to invaginate normally in mutant embryos. Late embryos show transformation of the optic lobe into Bolwig's organ; the number of cells in the Bolwig's organ is increased by a factor of 2-3 compared to wild type, while the optic lobe is absent.

Embryos lack all protocerebral neuroblasts of the anterior (Pa) and posterior (Pp) groups, while most central protocerebral (Pc) neuroblasts segregate normally. The protocerebrum is almost completely missing in late embryos.

Embryos lack abdominal segment 8 and have little or no hindgut.

Strong tll allele.

tlll49/Df(3R)tll-pgx embryos lack A8 and filzkorper.

Cuticular and brain defects.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Other
Statement
Reference
Phenotype Manifest In
Enhancer of
Statement
Reference

tll[+]/tlll49 is an enhancer of terminalia phenotype of kenok

Additional Comments
Genetic Interactions
Statement
Reference

tlll49 pros17 double mutant third instar larval mushroom body clones show reduced numbers of neurons (approximately 18.6) compared to controls (approximately 200 neurons) (this resembles a tll loss of function phenotype), while tlll49 pros17 double mutant non-mushroom body neuroblast clones show a tumour phenotype (this resembles a pros loss of function phenotype).

The frequency of terminal defects in kenok homozygous adults is increased by tlll49/+.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments

Mutant phenotype can be rescued to adulthood by P element mediated transformation of the wild type tll gene copy.

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

Strong tll allele.

Severity of the embryonic phenotype (deletion of either external structures, A8 or anal pads, or internal structures, hindgut) places tll alleles in the order: Df(3R)tll-pgx > tlll49 > tll1 > tlll29 > tll2 > tllle3.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (7)
References (27)