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General Information
Symbol
Dmel\tll1
Species
D. melanogaster
Name
FlyBase ID
FBal0016889
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
tllL10, tlll10-22
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Nucleotide change:
G30852768A
Reported nucleotide change:
G454A
Amino acid change:
C34Y | tll-PA
Reported amino acid change:
C34Y
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Polytene chromosomes normal.
Nature of the lesion
Statement
Reference
Amino acid replacement: C34Y. Nucleotide substitution: TGC to TAC. Residue is present in the first zinc finger.
Point mutation.
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
Detailed Description
Statement
Reference
MARCM clones of tll1 in the third instar mushroom bodies show a reduction in the number of labelled neurons to 17.2, compared to 200 in controls.
The hindgut of stage 15-16 mutant embryos is severely reduced, but endodermal parts of the midgut are covered with a thin sheet of visceral muscles.
The caudal visceral mesoderm primordium is missing.
hkb2 tll1 double mutant embryos show twisted gastrulation.
Embryos usually lack abdominal segment 8 and have little or no hindgut.
The hindgut is reduced and Malpighian tubules are missing in stage 14/15 embryos.
Strong tll allele.
Homozygous tll1 embryos from rlSem/+ mothers have a tll mutant phenotype.
Initial pattern of prd expression in the embryo drastically altered.
Embryonic defects cannot be suppressed by Dsor1Su1.
Disruption in gt expression patterns: the posterior domain extends posteriorly.
Does not interact with RpII140wimp maternal effect.
Suppression of tor13D embryos: increase in proportion of embryos that formed cuticle with denticles and decrease in proportion of embryos that formed empty sacs.
Homozygous embryos lack the most anterior and posterior structures; the head skeleton is smaller than normal and the Filzkorper, anal plate and spiracles are missing.
Filzkorper, posterior spiracles, anal tufts and anal pads are missing, anterior structures are indistinguishable from tll amorphic embryos. Small increase in segment length.
tll1 embryos have defects in the head skeleton, although the labrum is present. The Malpighian tubules, anal pads and segment A8 are missing. The posterior midgut, proctodeum and pole cells are normal.
Embryos transheterozygous for tll1 and either tlla, tllc or tlle have shortened pharyngeal ridges. A8 and the telson are missing. Homozygous tll1 embryos have no Malpighian tubules, but have a continuous gut that terminates at a clearly formed proctodeal opening at the dorsal posterior tip of the most posterior body segment (A7). One tracheal pit is missing, and the remaining pits appear more widely spaced on the dorsal side of the embryo than in wild-type. The main tracheal trunk ends abruptly at A6. Mature hemizygous tll1 embryos are of normal overall body length, due to an increase in the length of the abdominal segments that are present - this increase in segment length is seen as anteriorly as A2 and is most pronounced in A4, A5, A6 and A7 (becoming more pronounced more posteriorly).
embryonic lethal zygotic lethal with pattern deletions in anterior and posterior of embryo (but body of normal length due to increase in length of non-deleted pattern elements). Anteriorly, dorsal portion of cephalopharyngeal skeleton is defective (dorsal arms shortened, dorsal bridge unfused), dorsal pouch shortened and scleritized, much of brain missing. Posteriorly, eighth abdominal segment and telson, Malpighian tubules, hindgut and much of posterior midgut missing.
External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Enhancer of
Statement
Reference
Suppressor of
Other
Additional Comments
Genetic Interactions
Statement
Reference
Anterior-posterior polarization of cells in the extending germband is disrupted in kni10 hb4 fkh1 tll1 homozygous embryos.
tll1 svp1 double mutant clones in the wing show formation of ectopic vein tissue. This phenotype is approximately 100% penetrant and is cell autonomous.
bcd6 nosL7 tll1 embryos exhibit two telsons in mirror image. Injection of wild type posterior pole plasm induces formation of two mirror image abdomens.
Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (6)
Notes on Origin
Discoverer
Comments
Comments
The expression pattern of a variety of homeotic, pair-rule and gap genes in homozygous tll1 mutant embryos has been analysed.
The effects of the tll1 mutation on the spatial expression of hh and wg during embryogenesis have been investigated.
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 (5)
References (56)