Nucleotide substitution: C?T.
Substitution occurs at the beginning of the 'recognition helix' of the homeodomain.
Amino acid replacement: Q?term.
C21381606T
C?T|FBrf0058116
Q344term | tin-PA
Q?term
adult dorsal vessel (with tin346), with tinABD
adult heart (with tin346), with tinABD
adult heart (with tinR321N)
embryonic/larval aorta (with tin346), with tinABD
embryonic/larval heart (with tin346), with tinABD
embryonic/larval heart & mesoderm
transverse nerve & dorsal mesothoracic disc
transverse nerve & dorsal metathoracic disc
transverse nerve & dorsal prothoracic disc
tinEC40/+ flies do not exhibit a significantly increased pacing-induced heart failure rate.
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 ; 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 ; tinABD tin346/tinEC40 adults have a reduced lifespan compared to controls.
In tinEC40 mutant embryos, the lymph gland and heart fail to form.
Mutant embryos have defects in the forming mesoderm around the foregut, but do form foregut ectoderm. 65% of mutant embryos have excess cells in the dorsal midline of the b1 region of the embryonic brain; the area occupied by neuronal nuclei is increased compared to wild type. The preoral brain commissure is abnormally thin. At late embryonic stage 13, mutant embryos show a reduction in the number of apoptotic cells at the dorsal midline of the brain compared to wild type. The number of brain ganglionic mother cells is unaffected in stage 11 mutant embryos.
Mutant embryos have mild defects in the development of the tracheal dorsal trunk.
The ordered files of cells seen in wild-type midgut visceral muscle primordia are not seen in these mutant embryos. The meso18E staining cells appear to invaginate, however, movement towards the interior is ragged and no ordered file of cells form.
Visceral mesoderm and cardiac progenitors do not form in mutant embryos.
Heart and visceral mesoderm and a subset of the somatic muscle founders fail to form in tin mutant embryos.
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.
Only small islands of visceral mesoderm remain. Those principle midgut epithelial cells that are in contact with the islands of visceral mesoderm assume an epithelial phenotype.
Lack visceral muscles of the midgut though not the hindgut. The midgut constriction fail to form. The heart fails to develop: cardioblasts are not formed. Somatic muscle pattern is moderately affected, with the most extreme defect in the dorsal-most muscles.
tinEC40 has embryonic/larval tracheal dorsal trunk phenotype, enhanceable by zfh175.26
tinEC40 has embryonic/larval tracheal dorsal trunk phenotype, enhanceable by zfh165.34
tinABD, tinEC40 has embryonic cardioblast phenotype, non-enhanceable by edlk06602
tinABD, tinEC40 has heart primordium phenotype, non-enhanceable by edlk06602
tinEC40 has larval pericardial cell phenotype, suppressible by tin::Mmus\Nkx2-52.5HD-NK2SD.hs
tinEC40 has visceral trunk mesoderm phenotype, suppressible by Scer\GAL4twi.PB/Scer\GAL4Mef2.PR/Mmus\Nkx2-5UAS.cRa
tinEC40 has embryonic/larval heart & mesoderm phenotype, suppressible by Scer\GAL4twi.PB/Scer\GAL4Mef2.PR/Mmus\Nkx2-5UAS.cRa
tinEC40 has embryonic/larval heart & mesoderm phenotype, suppressible by tin::Mmus\Nkx2-5UAS.1-53:54-319/Scer\GAL4twi.PB/Scer\GAL4Mef2.PR
tinEC40 has visceral trunk mesoderm phenotype, suppressible by tin::Mmus\Nkx2-5UAS.Nkx-tin/Scer\GAL4twi.PB/Scer\GAL4Mef2.PR
tinEC40 has visceral trunk mesoderm phenotype, suppressible by Scer\GAL4twi.PB/Scer\GAL4Mef2.PR/tin::Mmus\Nkx2-5UAS.HDs
tinEC40 has embryonic/larval heart & mesoderm phenotype, suppressible by Scer\GAL4twi.PB/Scer\GAL4Mef2.PR/tin::Mmus\Nkx2-5UAS.HDs
tinEC40 has visceral trunk mesoderm phenotype, suppressible by Scer\GAL4twi.PB/tin::Mmus\Nkx2-5UAS.tin-Nkx/Scer\GAL4Mef2.PR
tinEC40 has embryonic/larval heart & mesoderm phenotype, suppressible by Scer\GAL4twi.PB/tin::Mmus\Nkx2-5UAS.tin-Nkx/Scer\GAL4Mef2.PR
tinEC40 has visceral trunk mesoderm phenotype, suppressible by Scer\GAL4twi.PB/Scer\GAL4Mef2.PR/tin::Mmus\Nkx2-5UAS.tin-HD,Nkx
tinEC40 has embryonic/larval heart & mesoderm phenotype, suppressible by Scer\GAL4twi.PB/Scer\GAL4Mef2.PR/tin::Mmus\Nkx2-5UAS.tin-HD,Nkx
tinEC40 has visceral trunk mesoderm phenotype, suppressible by Scer\GAL4twi.PB/Scer\GAL4Mef2.PR/tin::Mmus\Nkx2-5UAS.tin.1-220
tinEC40 has embryonic/larval heart & mesoderm phenotype, suppressible by Scer\GAL4twi.PB/Scer\GAL4Mef2.PR/tin::Mmus\Nkx2-5UAS.tin.1-220
tinEC40 has visceral trunk mesoderm phenotype, suppressible by tin::Mmus\Nkx2-5UAS.tin.1-134/Scer\GAL4twi.PB/Scer\GAL4Mef2.PR
tinEC40 has embryonic/larval heart & mesoderm phenotype, suppressible by tin::Mmus\Nkx2-5UAS.tin.1-134/Scer\GAL4twi.PB/Scer\GAL4Mef2.PR
tinEC40 has visceral trunk mesoderm phenotype, suppressible by Scer\GAL4twi.PB/Mmus\Nkx2-5UAS.ΔNK/Scer\GAL4Mef2.PR
tinEC40 has embryonic/larval heart & mesoderm phenotype, suppressible by Scer\GAL4twi.PB/Mmus\Nkx2-5UAS.ΔNK/Scer\GAL4Mef2.PR
tinABD, tinEC40 has embryonic cardioblast phenotype, non-suppressible by edlk06602
tinABD, tinEC40 has heart primordium phenotype, non-suppressible by edlk06602
tinEC40 has phenotype, non-suppressible by Scer\GAL4twi.PB/Scer\GAL4Mef2.PR/bapUAS.cRa
tinEC40 has phenotype, non-suppressible by Scer\GAL4twi.PB/Mmus\Nkx2-5UAS.ΔC/Scer\GAL4Mef2.PR
tinEC40 has phenotype, non-suppressible by Scer\GAL4twi.PB/Scer\GAL4Mef2.PR/Rnor\Nkx2-1UAS.cRa
tinEC40 is an enhancer of embryonic/larval tracheal dorsal trunk phenotype of zfh175.26
tinEC40 is an enhancer of embryonic/larval tracheal dorsal trunk phenotype of zfh165.34
tinEC40 is a suppressor | partially of visceral trunk mesoderm phenotype of Mmus\Nkx2-5UAS.cRa, Scer\GAL4Mef2.PR, Scer\GAL4twi.PB
tinEC40 is a suppressor | partially of embryonic/larval heart & mesoderm phenotype of Mmus\Nkx2-5UAS.cRa, Scer\GAL4Mef2.PR, Scer\GAL4twi.PB
Cdc42[+]/Cdc423, tinEC40 has adult heart phenotype
The formation of pericardial cells is restored when tin::Mmus\Nkx2-52.5HD-NK2SD.hs is expressed in tinEC40 embryos at 3.5 to 4.5 hours of development, although the cells are in a disorganised pattern.
Effect on visceral mesoderm can be rescued by Mmus\Nkx2-5Scer\UAS.cRa expression but not Rnor\TTF-1Scer\UAS.cRa nor bapScer\UAS.cRa. tin::Mmus\Nkx2-5Scer\UAS.1-53:54-319 and tinScer\UAS.ΔC fully rescue visceral mesoderm defect but only partially rescue cardiac mesoderm defects of tinEC40. Mmus\Nkx2-5Scer\UAS.cRa and tin::Mmus\Nkx2-5Scer\UAS.Nkx-tin partially suppress the visceral mesoderm defect but do not suppress the cardiac mesoderm defects of tinEC40. Mmus\Nkx2-5Scer\UAS.ΔNK partially suppresses both the visceral and the cardiac mesoderm defects of tinEC40.
tinEC40 is rescued by tinUAS.cRa/Scer\GAL4twi.PB/Scer\GAL4Mef2.PR
tinEC40 is partially rescued by tinUAS.ΔC/Scer\GAL4twi.PB/Scer\GAL4Mef2.PR
tinEC40 is partially rescued by Scer\GAL4twi.PB/tinUAS.Δ43-123/Scer\GAL4Mef2.PR
tinEC40 is not rescued by Scer\GAL4twi.PB/tinUAS.ΔHD/Scer\GAL4Mef2.PR
tinScer\UAS.Δ43-123 fully rescues visceral mesoderm defect but only partially rescues cardiac mesoderm defects of tinEC40.
Mohler and Pardue.