FB2024_03 , released June 25, 2024
Allele: Dmel\TrlR85
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General Information
Symbol
Dmel\TrlR85
Species
D. melanogaster
Name
FlyBase ID
FBal0034117
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
Trl85, R85
Key Links
Genomic Maps

Nature of the Allele
Progenitor genotype
Cytology
Description

Imprecise excision of the P-element and deletion of an extensive region of the Trl transcription unit.

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Comment:

Deletion resulting from imprecise P element excision. 20 base pairs remain from the 3' end of the transposon.

Variant Molecular Consequences
Associated Sequence Data
DNA sequence
Protein sequence
 
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

TrlR85/Trlex15 males are unable to produce viable offspring. The testes are 2-4 times smaller than normal and in 90% of cases only early stage (2- and 4-cell) germline cysts are present. Most of the mutant males have empty seminal vesicles, but 5% have a single mature, motile sperm. Mitochondrial defects are seen starting from the spermatogonia stage, with the mitochondria being much larger than normal, having a pale matrix and lacking cristae in many areas. At later stages of spermatogenesis autophagosome formation and massive lysis of the cytoplasm is seen.

Approximately 50% of TrlR85/Trl362 males are fertile, with seminal vesicles containing a small number of motile sperm. The testes are 1.5-3 times smaller than normal. Mitochondria are swollen and poorly condensed in spermatogonia and polar spermatocytes. Spermatocyte degradation is seen.

Defects in primordial germ cell (PGC) migration are seen in TrlR85/Trlex15 embryos. Some of the PGCs fail to migrate, and those that do are scattered throughout the embryo.

TrlR85/+ enhances the position effect variegation at the w locus which is seen in In(1)wm4 flies.

4% of heterozygous adult males show transformation of A6 to A5.

Cytoplasmic actin filaments are completely absent in 18% of TrlR85 mutant egg chambers, and the nurse cell nuclei block the ring canals.

Trlen82/TrlR85 mutant females lay one or two eggs per day, compared to 30-50 in wild type females. The size of the eggs varies from 320 to 400 micrometres, which is small compared to >500 micrometres seen in wild type flies. The eggs are elliptical and have short chorionic appendages.

Structural abnormalities are seen in the ovaries of Trlen82/TrlR85 mutant females from stage 10 of egg chamber development. Follicle cells are often localized to the posterior part of the oocyte and do not cover the posterior surface. Abnormal migration of centripetal cells is also seen. Many egg chambers contain oocytes of an irregular shape and many oocytes are localized in the nurse cell region. Not all cytoplasm from the nurse cells is transferred to the oocyte in many egg chambers, resulting in a 'dumpless' phenotype. Numerous degrading egg chambers are seen with abnormal chromatin condensation in the nurse cells at stages 9 and 10. This is not usually seen in wild type. Most nurse cells demonstrate no significant abnormalities in the structure of cytoplasmic actin filaments formed before the phase of rapid transport at stage 10B, however these filaments look thinner, less organised and are less evenly distributed over the chamber. Cytoplasmic actin filaments are completely absent in 1.8% of egg chambers, and the nurse cell nuclei block the ring canals in these egg chambers.

TrlR85 homozygous larvae do not reach third instar. TrlR85/Trl13C larvae do develop till third instar, though their imaginal discs are very small. When TrlR85 germ-line clones are made, only very few progeny are obtained. The phenotype of the few progeny obtained is variable, ranging from unfertilised eggs in most cases to embryos developing cuticle with various defects. The unfertilised eggs exhibit a defect in micropyle formation. Those embryos that are fertilised have completely defective anterior, and denticle belts are not properly formed. When TrlR85 somatic clones are made (in a Minute background) various phenotypes are seen. In general most clones display a lack of bristles and no clones present any obvious homeotic transformations. Clones in the eyes, the proboscis and palpi sometimes reduce their sizes. In the thorax, the notum is often split and there is a clear disappearance of both macrochaetae and microchaetae. In the wing margin, clones running along the dorsal-ventral border usually delete the triple row of bristles. Clones in the wing blade, produce wings with blisters, reduced sizes, and a "held-out" phenotype is sometimes seen. In legs, most of the clones show a lack of bristles, in the first leg of males, clones show a reduction of the number of sex comb hairs which invariably is accompanied by a lack of surrounding bristles in the clones.

TrlR85/+ does not suppress the variegation of lt due to In(2LR)ltG10 (seen in In(2LR)ltG10/Df(2L)lt10 animals derived from lt16/Df(2L)lt10 females); there is no significant change in the percentage of pigmented Malpighian tubule cells. TrlR85/+ does not suppress the variegation of lt due to In(2L)ltX2 (seen in In(2L)ltX2/Df(2L)lt10 animals derived from lt16/Df(2L)lt10 females); there is no significant change in the percentage of pigmented Malpighian tubule. TrlR85/+ enhances the variegation of lt due to T(2;3)ltX13 (seen in T(2;3)ltX13/Df(2L)lt10 animals derived from lt16/Df(2L)lt10 females), so that the percentage of pigmented Malpighian tubule cells is decreased in the double mutant larvae. TrlR85/+ does not suppress the variegation of lt due to In(2LR)ltG10 (seen in In(2LR)ltG10/lt1 animals); there is no significant change in the amount of eye pigment in the double mutant adults.

Heterozygotes do not have extra sex combs on the 2nd or 3rd leg and do not show transformation of antenna to leg.

Lethality occurs at hatching.

Does not effect position effect variegation at the bw locus caused by Byron.

Pairing sensitive repression is alleviated in iab-7 PRE lines that carry Trl13C.

Homozygotes die during the third larval instar with no obvious homeotic or other specific defects. Double homozygotes with z mutants show no cuticular defects.

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

TrlR85, Ubx130/Ubx[+] has homeotic phenotype, enhanceable by Taf3Fa4a

TrlR85, Ubx130 has visible phenotype, enhanceable by pho1

Trl[+]/TrlR85, Ubx130 has visible | dominant phenotype, enhanceable by +/Df(2R)Δ18

TrlR85, Ubx130/Ubx[+] has visible | dominant phenotype, enhanceable by +/Df(2R)Δ18

TrlR85 has visible phenotype, enhanceable by corto[+]/corto420

Enhancer of
Statement
Reference

Trl[+]/TrlR85 is an enhancer of visible | dominant | homeotic phenotype of Pc3

Trl[+]/TrlR85 is an enhancer of visible phenotype of corto420

Trl[+]/TrlR85 is an enhancer of visible | dominant | homeotic phenotype of brm[+]/brm2, trxE2

Trl[+]/TrlR85 is an enhancer of visible | dominant | homeotic phenotype of ash117, trxB11/trx[+]

Other
Phenotype Manifest In
Enhanced by
Statement
Reference

TrlR85, Ubx130/Ubx[+] has haltere phenotype, enhanceable by Taf3Fa4a

TrlR85, Ubx130/Ubx[+] has wing | ectopic phenotype, enhanceable by Taf3Fa4a

Trl[+]/TrlR85, Ubx130 has haltere phenotype, enhanceable by +/Df(2R)Δ18

Trl[+]/TrlR85, Ubx130 has wing | ectopic phenotype, enhanceable by +/Df(2R)Δ18

TrlR85, Ubx130/Ubx[+] has haltere phenotype, enhanceable by +/Df(2R)Δ18

TrlR85, Ubx130/Ubx[+] has wing | ectopic phenotype, enhanceable by +/Df(2R)Δ18

TrlR85 has humerus phenotype, enhanceable by corto[+]/corto420

NOT Enhanced by
Statement
Reference

TrlR85 has phenotype, non-enhanceable by Alhunspecified

NOT suppressed by
Statement
Reference

TrlR85 has phenotype, non-suppressible by Alhunspecified

Enhancer of
Statement
Reference

TrlR85 is an enhancer of haltere | ectopic phenotype of UbxCbx-1

TrlR85 is an enhancer of wing phenotype of UbxCbx-1

Trl[+]/TrlR85 is an enhancer of adult abdominal segment 4 | ectopic phenotype of E(z)Trm

Trl[+]/TrlR85 is an enhancer of adult abdominal segment 5 phenotype of E(z)Trm

Trl[+]/TrlR85 is an enhancer of adult mesothoracic segment | ectopic phenotype of E(z)Trm

Trl[+]/TrlR85 is an enhancer of adult prothoracic segment phenotype of E(z)Trm

Trl[+]/TrlR85 is an enhancer of antenna phenotype of Pc3

Trl[+]/TrlR85 is an enhancer of leg | ectopic phenotype of Pc3

Trl[+]/TrlR85 is an enhancer of mesothoracic leg phenotype of Pc3

Trl[+]/TrlR85 is an enhancer of metathoracic leg phenotype of Pc3

Trl[+]/TrlR85 is an enhancer of sex comb | ectopic phenotype of Pc3

Trl[+]/TrlR85 is an enhancer of humerus phenotype of corto420

Trl[+]/TrlR85 is an enhancer of adult metathoracic segment phenotype of brm[+]/brm2, trxE2

Trl[+]/TrlR85 is an enhancer of adult metathoracic segment phenotype of ash117, trxB11/trx[+]

Suppressor of
Statement
Reference

TrlR85 is a suppressor of eye phenotype of CycEJP

Trl[+]/TrlR85 is a suppressor of adult mesothoracic segment | ectopic phenotype of E(z)Trm

Trl[+]/TrlR85 is a suppressor of adult metathoracic segment phenotype of E(z)Trm

Trl[+]/TrlR85 is a suppressor of adult prothoracic segment phenotype of E(z)Trm

Other
Statement
Reference

KrIf-1, Trl[+]/TrlR85 has eye phenotype

Additional Comments
Genetic Interactions
Statement
Reference

Double heterozygosity for both polybromoΔ86 and TrlR85 enhances the position effect variegation at the w locus which is seen in In(1)wm4 flies more strongly than either single polybromoΔ86 and TrlR85 heterozygote alone.

12% of TrlR85/polybromoΔ86 and TrlR85/brm2 double heterozygous adult males show transformation of A6 to A5.

Homozygosity for TrlR85 slightly increases the eye colour in flies carrying wP1\loxP.ME.RW+.

Homozygosity for TrlR85 has no effect on the eye colour of flies carrying w-ME.RW+.

2.48% of flies carrying one copy of TrlR85 and one copy of Ubx130 show a mild haltere to wing transformation.

Homozygous bip2Fa4a does not enhance the frequency of haltere to wing transformation seen in TrlR85/TM2, Ubx130 flies (2.73% of flies show transformations, compared to 2.48%), but it does enhance the severity of the transformation.

Abd-BMcp-1, TrlR85 double heterozygotes have a partially pigmented abdominal segment 4. TrlR85/Ubx130; pho1 flies show an enhancement of the Ubx130 phenotype in 18% of flies. 37% of TrlR85/In(3R)Antprv1 flies show an antenna to leg phenotype, compared to the 25% observed in In(3R)Antprv1/+.

10+/-2% of KrIf-1/+ flies born to TrlR85/+ mothers have outgrowths with ectopic vibrissae protruding from the ventral region of the eye, compared to less than 0.1% of KrIf-1/+ flies born to isogenised wild-type mothers.

Mutant weakly suppresses the CycEJP rough eye phenotype.

Ubx130/TrlR85 flies have a low penetrance of haltere to wing transformations and notal transformations. The penetrance of these phenotypes is significantly enhanced by heterozygosity for Df(2R)Δ18.

45% of Pc3/TrlR85 double heterozygotes have extra sex combs (on the 2nd or 3rd leg) and 25% of Pc3/TrlR85 double heterozygotes show transformation of antenna to leg. 11% of TrlR85/+ ; pho1/+ double heterozygotes have extra sex combs (on the 2nd or 3rd leg) but they do not show transformation of antenna to leg.

corto420 TrlR85 double heterozygotes give a higher percentage of postpronotum defects than expected for an additive phenotype, indicating a synergistic interaction.

Double heterozygotes with ash122, trxB11 or brm2 show T3 to T2 transformations.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Not rescued by
Comments

Expression of TrlHsp83.GAGA-581 rescues the egg chamber phenotypes seen in Trlen82/TrlR85 mutant females.

Expression of TrlHsp83.GAGA-519 rescues the egg chamber phenotypes seen in Trlen82/TrlR85 mutant females.

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

Attempts to make germ-line clones with this allele failed.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (7)
References (44)