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FB2026_01
,
released March 12, 2026
NK-4, msh-2, NK4/msh-2, NK4, msh2
transcription factor - homeodomain - NK-2 class - mesodermal - involved in the formation of the heart and dorsal vascular musculature
Please see the JBrowse view of Dmel\tin for information on other features
To submit a correction to a gene model please use the Contact FlyBase form
AlphaFold produces a per-residue confidence score (pLDDT) between 0 and 100. Some regions with low pLDDT may be unstructured in isolation.
Gene model reviewed during 5.49
1.8 (northern blot)
1.7 (northern blot)
There is only one protein coding transcript and one polypeptide associated with this gene
416 (aa)
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\tin using the Feature Mapper tool.
The testis specificity index was calculated from modENCODE tissue expression data by Vedelek et al., 2018 to indicate the degree of testis enrichment compared to other tissues. Scores range from -2.52 (underrepresented) to 5.2 (very high testis bias).
Comment: anlage in statu nascendi
Comment: anlage in statu nascendi
tin is first expressed between 2 and 4 hours of embryogenesis, peaks between 4 and 8 hours and decreases dramatically in late embryogenesis. It is not expressed postembryonically. tin is first expressed in the cellular blastoderm embryo in the ventral-most region of the embryo. After invagination of the ventral-most cells, tin mRNA is found exclusively in the mesoderm. During stage 9, tin expression is reduced in some mesodermal cells and by stage 10, tin expression is restricted to 6-8 cells on either side in the dorsal-most reigons of the mesoderm. During stage 11, each tin-expressing region splits into two separate domains. One corresponds to part of the visceral mesoderm and the other to cells at the dorsal tip of the mesoderm that include the precursors to the heart. tin expression continues in heart progenitors until late stages of embryogenesis when they differentiate into the dorsal blood vessel.
tin transcripts are expressed predominantly between 3 and 9 hours of embryogenesis and are present at low levels between 9 and 12 hours. They are first expressed along the ventral longitudinal axis in the late blastoderm just prior to the ventral invagination of the mesoderm. The strip of tin-expressing cells is about 14-16 cells wide. After gastrulation, tin is expressed in the mesoderm. At about 4.5 hours, the mesodermal mass starts to spread dorsally. As the cell layer reaches the dorsal margin, ventrally located mesodermal cells cease tin expression. The dorsally located cells which are the primordia for the visceral musculature express tin for another 1-2 hours. In stage 11, tin expression in the dorsal mesoderm is reduced to patches of cells. tin expression is also seen in the cephalic region at ~stage 10-11 surrounding the stomodeum. In stage 11, a row of cells at the dorsal margin begins expressing tin. These cells which correspond to heart primordia, are the only ones that continue to express tin after the germ band extended stage.
Comment: excluded from srp-expressing region
Prior to embryonic stage 12, the cardiogenic mesoderm, defined by the expression of tin, forms segmentally reiterated, elongated clusters of approximately 30-35 cells each in the early cardiogenic mesoderm. This number increases to about 60 at the end of stage 12. Based on cell size and shape and the expression levels of Dl, dorsal and ventral subdomains within the cardiogenic mesoderm of stage 12 embryos can be distinguished. Cells of the ventral domain are small and express moderate levels of Dl and tin. Dorsally, larger cells, expressing higher levels of tin are observed.
tin protein is expressed in cardial, but not pericardial, cells in third instar larvae.
tin protein is observed in the cephalic vascular rudiment, a group of cells surrounding the migrating corpus cardiacum precursor cells, and that represent an evolutionary vestige of the cephalic aorta.
Expression of tin protein is observed in four pairs of cardioblasts per thoracic hemisegment, and in the posterior-most four pairs of cardioblasts per abdominal hemisegment.
Four pairs of tin-positive nuclei are seen in the larval heart but none are in the region of the ostia.
tin protein is detected in the trunk mesoderm at stage 8-9, the dorsal mesoderm at stage 10, and the cardiac and visceral mesoderm at stage 11-12. After stage 14, expression is restricted to the developing heart. In stage 15-16 embryos, expression is detected in the myocardial and pericardial cells of the heart tube, with only 4 out of 6 cells per hemisegment expressing tin protein.
JBrowse - Visual display of RNA-Seq signals
View Dmel\tin in JBrowse
3-71
3-74.1
Please Note FlyBase no longer curates genomic clone accessions so this list may not be complete
Please Note This section lists cDNAs and ESTs that fall within the genomic extent of the gene model, which may include cDNAs and ESTs of genes within introns, or of overlapping genes. Please see JBrowse for alignment of the cDNAs and ESTs to the gene model.
For each fully sequenced cDNA the DGRC maintains various forms of the cDNA (e.g tagged or untagged) in several different host vectors for subsequent cloning and expression in Drosophila and Drosophila cell lines.
DNA-protein interactions: genome-wide binding profile assayed for tin protein in stage 9-11 embryos; ArrayExpress accession number E-MTAB-1184.
tin is required for the development of all cardiogenic mesoderm.
tin is not required for early zfh1 expression throughout the mesoderm or for the refinement of this expression to lateral mesodermal clusters during stage 10. tin activity is required for aspects of zfh1 expression beginning at stage 11. tin and zfh1 cooperate in the specification of two tissues derived from the lateral mesoderm: the gonadal mesoderm and the fat body.
Mutants are isolated in an EMS mutagenesis screen to identify zygotic mutations affecting germ cell migration at discrete points during embryogenesis: mutants exhibit germ cell migration defects.
tin is required for the development of both fat body and gonadal mesoderm in the embryo.
While tin and Mmus\Nkx2-5 show close functional kinship, their mode of deployment in cardiogenesis has diverged possibly because of differences in their interactions with accessory factors. The distinct cardiogenic programs in vertebrates and flies may be built upon a common and perhaps more ancient program for the specification of visceral muscle.
tin is involved in the regionalisation of the dorsolateral mesoderm by the homeotic genes. There is a balance between fat body and somatic gonadal precursor (SGP) development with tin, wg and en driving cells in the primary clusters towards SGP development and srp driving them towards fat body development.
Two distinct clusters of E-box regulatory sequences, present upstream of tin, mediate tin expression in the visceral mesoderm. These elements are conserved between tin and Dvir\tin and serve as binding sites for twi (E1 cluster) and tin (E2 cluster). Results demonstrate tin is a direct transcriptional target for twi and its own gene product in visceral mesodermal cells, supporting the idea that twi and tin function in the subdivision of the mesoderm during embryogenesis.
tin is controlled by an array of discrete enhancer elements that are activated successively by differential genetic inputs, as well as by closely linked activator and repressor binding sites within an early-acting enhancer, which restricts twi activity to specific areas within the twi expression domain. Three of the four identified elements are conserved between D.melanogaster and D.virilis with respect to sequence, relative position and spatial/temporal activity. Overall orientation not stated: mod(mdg4)- tin+
An inductive signal from dorsal ectodermal cells is required for activation of tin in the underlying mesoderm. dpp serves as a signalling molecule in this process. The spatial expression of dpp in the ectoderm determines which cells of the mesoderm become competent to develop into visceral mesoderm and the heart.
Observations of tin mutants suggest that transverse nerve exit glial cell are required for axon pathfinding in the embryo, and that these glia and the support cells of the dorsal neurohemal organs have a mesodermal origin.
Genetic analysis demonstrates that the tin gene product is required for the formation of visceral musculature, the specification of heart precursor cells and the normal development of body wall muscles from the dorsal mesoderm.
The function of tin is required for visceral muscle and heart development, though somatic muscle development is largely unaffected in mutants.
In mutant embryos lacking the entire mesoderm or failing to differentiate the visceral mesoderm, the anterior and posterior midgut primordia form but do not migrate properly.
tin acts after the initial mesoderm induction downstream of twi and is likely to specify primordial cell fates of the heart and visceral muscles.
tin has been cloned and characterised.
The tin homeobox gene is first expressed in 3-hour embryos; no tin mRNA is detected in embryos at earlier stages of development. tin mRNA is detected only in mesodermal cells. The transcripts are most abundant in 3-9-hour embryos; the mRNA decreases in abundance thereafter.
May be allelic to l(3)93Dg.
