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General Information
Symbol
Dmel\tin346
Species
D. melanogaster
Name
FlyBase ID
FBal0035787
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
tin34B
Key Links
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Small deletion of 130bp within the tin transcription unit.

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

embryonic/larval fat body & parasegment 3

embryonic/larval fat body & parasegment 13

gonad & parasegment 10

gonad & parasegment 11

gonad & parasegment 12

myofibril & adult dorsal vessel (with tinEC40), with tinABD

myofibril & larval dorsal vessel (with tinEC40), with tinABD

myofibril & larval heart (with tinEC40), with tinABD

transverse nerve & dorsal mesothoracic disc

transverse nerve & dorsal metathoracic disc

transverse nerve & dorsal prothoracic disc

Detailed Description
Statement
Reference

Mutants show loss of expression of P{FMRFa-EGFP.Tv}, a marker for the six Ap4 neurons in the developing ventral nerve cord, and loss of expression of eya, which identifies the four Ap cluster neurons.

tin346/+ flies do not exhibit a significantly increased pacing-induced heart failure rate.

Homozygous embryos show defects in the normal left-right asymmetry of the anterior midgut, with many showing either inversion of the normal asymmetry or no left-right asymmetry.

The myofibrils of the dorsal vessel are arranged almost exclusively in an anterior-posterior orientation in tinABD ; tin346/tinEC40 larvae, in contrast to wild-type larvae where they are arranged spirally. In the posterior heart region of the dorsal vessel the pattern of myofibrils is highly irregular in the mutant larvae, forming abnormal cross-shaped or 'knotted' patterns. The aorta appears thinner than normal in the mutant larvae, whereas the heart frequently has a wider diameter than normal.

The heart tube is much thinner than normal in tinABD ; tin346/tinEC40 adults. The mutant myofibrils are arranged longitudinally and transverse spirally arranged myofibrils are almost completely absent.

tinABD ; tin346/tin346 and tinABD ; tinABD tin346/tinEC40 adults show a dramatic increase in heart failure rate after pacing of the heart by external electrical stimulus compared to the heart failure rate of control adults. The recovery rate after heart failure is dramatically decreased in the mutant adults.

tinABD ; tin346/tin346 and tinABD ; tinABD tin346/tinEC40 adults have a reduced lifespan compared to controls.

tin346 mutants show a salivary gland phenotype. At stage 14, mutant salivary glands remain associated with the inner circular muscle layer, while in wild type, these structures become separate. After stage 15, cells from the distal tips of the tin346 salivary glands spread into the region of the undifferentiated midgut that forms the gastric caecae in wild-type embryos. The mutant glands become mispositioned and/or elongated and maintain contact with the area of the midgut immediately adjacent to the proventriculus.

In stage-15 tin346 mutant embryos, the lymph gland, cardioblasts and pericardial nephrocytes fail to develop from the cardiogenic mesoderm.

In tin45/tin346 mutants the dorsal neurohemal organs (DNHs) are absent.

A Fas3-positive visceral mesoderm-like structure is present in parasegments 1 through 4 in mutant embryos. The majority of distal salivary cells initiate posterior migration during stage 12, as occurs in wild-type embryos. However, the posterior migration of the salivary glands in the mutant embryos does not always follow the normal path close to the body wall and instead, the glands of late embryos are observed in random positions, often as bent tubes.

Migration of the mesoderm is normal in early embryos.

Ectopic fat body precursors arise in parasegments 10-12: transformation of somatic gonadal precursor (SGP) cells into primary fat body clusters. Also the large fat body cluster in the dorsal region of parasegment 13 is lost and fat body cells can be detected only in the dorsolateral mesoderm. An additional fat body cluster appears late in parasegment 3.

Muscles 18 are enlarged in homozygous embryos and extend into areas where dorsal body wall muscles are normally located.

Few or no somatic gonadal precursor cells are specified.

Some homozygous embryos hatch and survive as first instar larvae, even though they have midgut and body wall muscle defects. They fail to grow and show lethargic behavior and large midguts. The transverse nerve is missing, as are the dorsal neurohemal organs. Both the dorsal and ventral lateral bipolar dendrite neuron are disrupted when the transverse nerve is not formed. Segmental nerve b target muscles are abnormally innervated, and this is often associated with the loss of some muscle fibres. Transverse nerve exit glial cell cannot be found.

Strong mesodermal phenotype: midgut musculature is completely missing, midgut, foregut, proventriculus and hindgut appear normal. The pattern of body wall muscles is disrupted due to the absence of muscle founder cells. In the absence of visceral mesoderm the endoderm fails to migrate. The cardioblasts and pericardial cells are absent.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
NOT Enhancer of
Statement
Reference

tin346/tin[+] is a non-enhancer of adult heart phenotype of pnrVX6

tin346/tin[+] is a non-enhancer of adult heart phenotype of pnr1

tin346/tin[+] is a non-enhancer of adult heart phenotype of pnrVX1e

NOT Suppressor of
Statement
Reference

tin346/tin[+] is a non-suppressor of adult heart phenotype of pnrVX6

tin346/tin[+] is a non-suppressor of adult heart phenotype of pnr1

tin346/tin[+] is a non-suppressor of adult heart phenotype of pnrVX1e

Other
Additional Comments
Genetic Interactions
Statement
Reference

tin346/+ ; Df(3R)Exel6157/+ double heterozygous embryos show asymmetric cell division defects in "svp" cardiac progenitor cells that are significantly more severe than the additive effects of each of the two single heterozygotes. Defects in the symmetric cell divisions that give rise to the tin-expressing cardial cells are also significantly more severe in the double heterozygotes.

tin346/+ ; Df(1)CHES-1-like1/+ double heterozygous embryos show asymmetric cell division defects in "svp" cardiac progenitor cells that are significantly more severe than the additive effects of each of the two single heterozygotes. Defects in the symmetric cell divisions that give rise to the tin-expressing cardial cells are also significantly more severe in the double heterozygotes.

tin346/+; Df(1)Exel6244/+ double heterozygotes, tin346/+; Df(1)Exel6242/+ double heterozygotes, tin346/+; Df(1)Exel6290/+ double heterozygotes, tin346/+; Df(1)Exel9067/+ double heterozygotes, tin346/+; Df(1)ED429/+ double heterozygotes, tin346/+; Df(2L)Exel6002/+ double heterozygotes, and tin346/+; Df(2L)Exel6016/+ double heterozygotes exhibit increased pacing-induced heart failure rate.

tin346/+; Df(1)Exel6253/+ double heterozygotes exhibit a significantly increased pacing-induced heart failure rate, arrhythmia and longer diastolic intervals, in addition to severe misalignment of cardiac myofibrils, as compared with controls. These flies do not exhibit differences in systolic intervals.

tin346/+; Df(2L)Exel7011/+ double heterozygotes are embryonic lethal.

tin346/+; Cdc423/+ double heterozygotes exhibit a significantly increased pacing-induced heart failure rate, significantly increased arrhythmia and a tendency toward longer diastolic intervals, in addition to severe misalignment of cardiac myofibrils, as compared with controls. These flies do not exhibit differences in systolic intervals.

The increase in heart arrest/fibrillation upon electrical pacing that is seen in pnrVX1e/+, pnr1/+ or pnrVX6/+ adults is not significantly altered by tin346/+.

The pacing-induced heart arrest/fibrillation rate for Df(2L)Exel6012/+; tin346/+ is dramatically elevated compared to the single heterozygous controls. This phenotype can be rescued by expressing midScer\UAS.cQb specifically in the heart with Scer\GAL4tin.CΔ4. An interaction of Df(2L)Exel6012/+; tin346/+ is also observed with respect to the development of arrhythmias, the level of cardiac expression of potential downstream effector genes, and the alignment of myofibers within the cardiac myocytes.

Df(3L)29A6; Df(3L)DocA, tin346 stage 16 embryos have a reduced number of cardioblasts compared to wild type; Df(3L)29A6; Df(3L)DocA, pnrVX6, tin346 embryos have even fewer cardioblasts and form only short regions of the dorsal vessel. Df(3L)29A6; pnrVX6, tin346 show a milder loss of cardioblasts.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Rescued by
Partially rescued by

tin346 is partially rescued by tinABD

Comments
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
References (43)