FlyBase Allele Report: Dmel\tin[346]

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.

(Bivik et al., 2015)

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

(Qian et al., 2011)

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.

(Taniguchi et al., 2007)

The myofibrils of the dorsal vessel are arranged almost exclusively in an anterior-posterior orientation in tin^ABD ; tin³⁴⁶/tin^EC40 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 tin^ABD ; tin³⁴⁶/tin^EC40 adults. The mutant myofibrils are arranged longitudinally and transverse spirally arranged myofibrils are almost completely absent.

tin^ABD ; tin³⁴⁶/tin³⁴⁶ and tin^ABD ; tin^ABD tin³⁴⁶/tin^EC40 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.

tin^ABD ; tin³⁴⁶/tin³⁴⁶ and tin^ABD ; tin^ABD tin³⁴⁶/tin^EC40 adults have a reduced lifespan compared to controls.

(Zaffran et al., 2006)

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.

(Vining et al., 2005)

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

(Mandal et al., 2004)

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

(Allan et al., 2003)

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.

(Bradley et al., 2003)

Migration of the mesoderm is normal in early embryos.

(Michelson et al., 1998)

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.

(Riechmann et al., 1998)

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

(Yin and Frasch, 1998)

Few or no somatic gonadal precursor cells are specified.

(Boyle et al., 1997)

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.

(Gorczyca et al., 1994)

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.

(Azpiazu and Frasch, 1993)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Other

Statement

Reference

Df(2L)Exel7011/+, tin³⁴⁶ has lethal - all die during embryonic stage phenotype

(Qian et al., 2011)

Df(3L)29A6, Df(3L)DocA, pnr^VX6, tin³⁴⁶ has lethal phenotype

(Reim and Frasch, 2005)

Df(3L)DocA, pnr^VX6, tin³⁴⁶ has viable phenotype

(Reim and Frasch, 2005)

Phenotype Manifest In

NOT Enhancer of

Statement

Reference

tin³⁴⁶/tin[+] is a non-enhancer of adult heart phenotype of pnr^VX6

(Qian and Bodmer, 2009)

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

(Qian and Bodmer, 2009)

tin³⁴⁶/tin[+] is a non-enhancer of adult heart phenotype of pnr^VX1e

(Qian and Bodmer, 2009)

NOT Suppressor of

Statement

Reference

tin³⁴⁶/tin[+] is a non-suppressor of adult heart phenotype of pnr^VX1e

(Qian and Bodmer, 2009)

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

(Qian and Bodmer, 2009)

tin³⁴⁶/tin[+] is a non-suppressor of adult heart phenotype of pnr^VX6

(Qian and Bodmer, 2009)

Other

Statement

Reference

Df(3R)Exel6157/+, tin³⁴⁶ has cardiogenic mesoderm phenotype

(Ahmad et al., 2012)

Df(1)CHES-1-like¹/+, tin³⁴⁶ has cardiogenic mesoderm phenotype

(Ahmad et al., 2012)

Df(1)Exel6244/+, tin³⁴⁶ has adult heart phenotype

(Qian et al., 2011)

Df(1)Exel6253/+, tin³⁴⁶ has adult heart phenotype

(Qian et al., 2011)

Df(1)Exel6253/+, tin³⁴⁶ has cardial cell phenotype

(Qian et al., 2011)

Df(1)Exel6253/+, tin³⁴⁶ has cardiac myofibril phenotype

(Qian et al., 2011)

Df(1)Exel6242/+, tin³⁴⁶ has adult heart phenotype

(Qian et al., 2011)

Df(1)Exel6290/+, tin³⁴⁶ has adult heart phenotype

(Qian et al., 2011)

Df(1)Exel9067/+, tin³⁴⁶ has adult heart phenotype

(Qian et al., 2011)

Df(1)ED429/+, tin³⁴⁶ has adult heart phenotype

(Qian et al., 2011)

Df(2L)Exel6002/+, tin³⁴⁶ has adult heart phenotype

(Qian et al., 2011)

Df(2L)Exel6016/+, tin³⁴⁶ has adult heart phenotype

(Qian et al., 2011)

Cdc42[+]/Cdc42³, tin³⁴⁶ has adult heart phenotype

(Qian et al., 2011)

Cdc42[+]/Cdc42³, tin³⁴⁶ has cardial cell phenotype

(Qian et al., 2011)

Cdc42[+]/Cdc42³, tin³⁴⁶ has cardiac myofibril phenotype

(Qian et al., 2011)

Df(3L)29A6, Df(3L)DocA, pnr^VX6, tin³⁴⁶ has cardioblast phenotype

(Reim and Frasch, 2005)

Df(3L)29A6, Df(3L)DocA, pnr^VX6, tin³⁴⁶ has embryonic/larval dorsal vessel phenotype

(Reim and Frasch, 2005)

Df(3L)29A6, pnr^VX6, tin³⁴⁶ has cardioblast phenotype

(Reim and Frasch, 2005)

Df(3L)29A6, Df(3L)DocA, tin³⁴⁶ has cardioblast phenotype

(Reim and Frasch, 2005)

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.

(Ahmad et al., 2012)

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.

(Qian et al., 2011)

The increase in heart arrest/fibrillation upon electrical pacing that is seen in pnr^VX1e/+, pnr¹/+ or pnr^VX6/+ adults is not significantly altered by tin³⁴⁶/+.

(Qian and Bodmer, 2009)

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 mid^Scer\UAS.cQb specifically in the heart with Scer\GAL4^tin.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.

(Qian et al., 2008)

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, pnr^VX6, tin³⁴⁶ embryos have even fewer cardioblasts and form only short regions of the dorsal vessel. Df(3L)29A6; pnr^VX6, tin³⁴⁶ show a milder loss of cardioblasts.

(Reim and Frasch, 2005)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Rescued by

tin³⁴⁶ is rescued by tin^+t10.7

(Azpiazu and Frasch, 1993)

Partially rescued by

tin³⁴⁶ is partially rescued by tin^ABD

(Zaffran et al., 2006)

Comments

Images (0)

Mutant

Wild-type

Stocks (2)

Bloomington

603840

w^*; P{neoFRT}82B pnr^VX6 e^s tin³⁴⁶ ca¹/TM3, P{eve-lacZ8.0}AG1, Sb¹

92964

w^*; ru¹ Diap1^th-1 st¹ kni^ri-1 rn^roe-1 p^p e^s tin³⁴⁶ ca¹/TM3, P{GAL4-twi.G}2.3, P{UAS-2xEGFP}AH2.3, Sb¹ Ser¹

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (3)

Reported As

Symbol Synonym

tin^34B

(Sellin et al., 2006)

tin^34b

(Bivik et al., 2015)

Name Synonyms

Secondary FlyBase IDs

References (45)

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