FlyBase Allele Report: Dmel\tll[1]

General Information

Symbol

Dmel\tll¹

Species

D. melanogaster

Name

FlyBase ID

FBal0016889

Feature type

allele

Associated gene

Dmel\tll

Associated Insertion(s)

Carried in Construct

Also Known As

tll^L10, tll^l10-22

Key Links

Genomic Maps

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Allele class

loss of function allele

hypomorphic allele - genetic evidence

Mutagen

ethyl methanesulfonate

Nature of the Allele

Allele class

hypomorphic allele - genetic evidence

(Wang et al., 2006, Kraut and Levine, 1991, Strecker et al., 1988)

loss of function allele

(Kraut and Levine, 1991)

Mutagen

ethyl methanesulfonate

(Diaz et al., 1996, Tearle and Nusslein-Volhard, 1987, Strecker et al., 1986)

Mutations Mapped to the Genome

Type

Location

Additional Notes

References

point_mutation

3R:30,852,768..30,852,768 [+]

Nucleotide change:

G30852768A

Reported nucleotide change:

G454A

Amino acid change:

C34Y | tll-PA

Reported amino acid change:

C34Y

(Diaz et al., 1996)

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

Progenitor genotype

Cytology

Polytene chromosomes normal.

(Strecker et al., 1986)

Nature of the lesion

Statement

Reference

Amino acid replacement: C34Y. Nucleotide substitution: TGC to TAC. Residue is present in the first zinc finger.

(Diaz et al., 1996)

Point mutation.

(Margolis et al., 1995)

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 neuroanatomy | somatic clone

(Kurusu et al., 2009)

lethal | recessive

(Strecker et al., 1986)

lethal - all die during embryonic stage | recessive

(Diaz et al., 1996, Tearle and Nusslein-Volhard, 1987)

some die during embryonic stage | recessive

(Diaz et al., 1996, Tearle and Nusslein-Volhard, 1987)

Phenotype Manifest In

abdominal segment 2

(Strecker et al., 1986)

abdominal segment 3

(Strecker et al., 1986)

abdominal segment 4

(Strecker et al., 1986)

abdominal segment 5

(Strecker et al., 1986)

abdominal segment 6

(Strecker et al., 1986)

abdominal segment 7

(Strecker et al., 1986)

abdominal segment 8

(Diaz et al., 1996, Strecker et al., 1986)

anal pad

(Tearle and Nusslein-Volhard, 1987)

cephalopharyngeal skeleton

(Lehmann, 1988, Tearle and Nusslein-Volhard, 1987)

embryonic/larval anus | embryonic stage

(Lehmann, 1988)

embryonic/larval hindgut | embryonic stage

(Diaz et al., 1996, Harbecke and Lengyel, 1995)

embryonic/larval posterior spiracle | embryonic stage

(Lehmann, 1988)

embryonic abdominal segment 8

(Tearle and Nusslein-Volhard, 1987)

embryonic hindgut

(Wolfstetter et al., 2009)

filzkorper

(Lehmann, 1988)

longitudinal visceral muscle primordium

(Kusch and Reuter, 1999)

Malpighian tubule

(Harbecke and Lengyel, 1995, Strecker et al., 1986)

Malpighian tubule primordium

(Tearle and Nusslein-Volhard, 1987)

mushroom body neuroblast | somatic clone

(Kurusu et al., 2009)

telson

(Strecker et al., 1986)

tracheal pit

(Strecker et al., 1986)

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.

(Kurusu et al., 2009)

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.

(Wolfstetter et al., 2009)

The caudal visceral mesoderm primordium is missing.

(Kusch and Reuter, 1999)

hkb² tll¹ double mutant embryos show twisted gastrulation.

(Yip et al., 1997)

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

(Diaz et al., 1996)

The hindgut is reduced and Malpighian tubules are missing in stage 14/15 embryos.

(Harbecke and Lengyel, 1995)

Strong tll allele.

(Margolis et al., 1995)

Homozygous tll¹ embryos from rl^Sem/+ mothers have a tll mutant phenotype.

(Brunner et al., 1994)

Initial pattern of prd expression in the embryo drastically altered.

(Gutjahr et al., 1993)

Embryonic defects cannot be suppressed by Dsor1^Su1.

(Tsuda et al., 1993)

Disruption in gt expression patterns: the posterior domain extends posteriorly.

(Kraut and Levine, 1991)

Does not interact with RpII140^wimp maternal effect.

(Parkhurst and Ish-Horowicz, 1991)

Suppression of tor^13D embryos: increase in proportion of embryos that formed cuticle with denticles and decrease in proportion of embryos that formed empty sacs.

(Strecker et al., 1991)

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.

(Lehmann, 1988)

Filzkorper, posterior spiracles, anal tufts and anal pads are missing, anterior structures are indistinguishable from tll amorphic embryos. Small increase in segment length.

(Strecker et al., 1988)

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.

(Tearle and Nusslein-Volhard, 1987)

Embryos transheterozygous for tll¹ and either tll^a, tll^c or tll^e 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).

(Strecker et al., 1986)

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

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Other

Statement

Reference

fkh¹, hb⁴, kni¹⁰, tll¹ has abnormal cell polarity | gastrula stage phenotype

(Zallen and Wieschaus, 2004)

svp¹, tll¹ has visible | somatic clone phenotype

(Gritzan et al., 2002)

Phenotype Manifest In

Enhancer of

Statement

Reference

tll¹ is an enhancer of wing vein | ectopic phenotype of Scer\GAL4^32B, rl^Sem.C.UAS

(Gritzan et al., 2002)

Suppressor of

Statement

Reference

tll¹ is a suppressor | maternal effect of embryonic/first instar larval cuticle | maternal effect phenotype of tor^12D

(Li and Li, 2003)

Other

Statement

Reference

svp¹, tll¹ has wing vein | ectopic | somatic clone | cell autonomous phenotype

(Gritzan et al., 2002)

svp¹, tll¹ has wing | somatic clone | cell autonomous phenotype

(Gritzan et al., 2002)

bcd⁶, nos^L7, tll¹ has epidermis phenotype

(Lehmann and Frohnhofer, 1989)

bcd⁶, nos^L7, tll¹ has telson phenotype

(Lehmann and Frohnhofer, 1989)

Additional Comments

Genetic Interactions

Statement

Reference

Anterior-posterior polarization of cells in the extending germband is disrupted in kni¹⁰ hb⁴ fkh¹ tll¹ homozygous embryos.

(Zallen and Wieschaus, 2004)

tll¹ svp¹ double mutant clones in the wing show formation of ectopic vein tissue. This phenotype is approximately 100% penetrant and is cell autonomous.

(Gritzan et al., 2002)

bcd⁶ nos^L7 tll¹ embryos exhibit two telsons in mirror image. Injection of wild type posterior pole plasm induces formation of two mirror image abdomens.

(Lehmann and Frohnhofer, 1989)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Rescued by

tll¹ is rescued by Scer\GAL4^elav-C155/tll^UAS.cKa

(Kurusu et al., 2009)

Comments

Images (0)

Mutant

Wild-type

Stocks (6)

Bloomington

2729

st¹ e¹ tll¹/TM3, Sb¹

3310

st¹ tsl³ tll¹/TM3, Sb¹

3335

Diap1¹ st¹ kni^ri-1 p^p pum³ e¹ tll¹/TM3, Sb¹

3309

Diap1¹ st¹ cp¹ in¹ kni⁶ kni^ri-1 p^p e¹ tll¹/TM3, Sb¹ Ser¹

Kyoto

107449

st¹ e¹ tll¹/TM3, Sb¹

106986

Diap1¹ st¹ kni^ri-1 p^p pum³ e¹ tll¹/TM3, Sb¹

Notes on Origin

Discoverer

Comments

The expression pattern of a variety of homeotic, pair-rule and gap genes in homozygous tll¹ mutant embryos has been analysed.

(Reinitz and Levine, 1990)

The effects of the tll¹ mutation on the spatial expression of hh and wg during embryogenesis have been investigated.

(Mohler, 1995)

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 > tll^l49 > tll¹ > tll^l29 > tll² > tll^le3.

(Diaz et al., 1996)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (5)

Reported As

Symbol Synonym

tll¹

(Rives-Quinto et al., 2020, Crossman et al., 2018, Liang et al., 2012, Kurusu et al., 2009, Wolfstetter et al., 2009, Sanders et al., 2008, Haecker et al., 2007, Sprecher et al., 2007, Wang et al., 2006)

tll^L10-22

(Mohler, 1995)

tll^l10-22

(Beller et al., 2002, Beller et al., 2002)

Name Synonyms

tailless1

(Sanders et al., 2008)

Secondary FlyBase IDs

References (58)

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