A role for the COUP-TF-related gene seven-up in the diversification of cardioblast identities in the dorsal vessel of Drosophila

• Published in: Mechanisms of development 2001-06, Vol.104 (1), p.49-60
• Main Authors: Lo, Patrick C.H, Frasch, Manfred
• Format: Article
• Language: English
• Subjects: Animals; Cardioblasts; COUP Transcription Factor I; DNA-Binding Proteins - physiology; Drosophila - embryology; Drosophila heart; Drosophila Proteins; Genes, Reporter; Heart - embryology; In Situ Hybridization; Microscopy, Confocal; Mutation; Myocardium - cytology; Receptors, Steroid - physiology; Repressor Proteins - metabolism; RNA, Messenger - metabolism; seven-up; tinman; Tissue Distribution; Trans-Activators - metabolism; Transcription Factors - physiology
• ISSN: 0925-4773; 1872-6356
• DOI: 10.1016/S0925-4773(01)00361-6

The Drosophila gene tinman is essential for dorsal vessel (heart) formation and is structurally and functionally conserved in vertebrates. In the mature embryonic dorsal vessel, tinman is expressed in four of the six pairs of cardioblasts in each segment. We provide evidence that seven-up, which is homologous to the vertebrate COUP-TF transcription factor and is expressed in the non-Tinman-expressing cardioblasts, represses tinman in these cells. Loss of function seven-up mutations derepress tinman expression in these cardioblasts while ectopic expression of seven-up represses tinman in the cardioblasts that normally express it. These changes are correlated with alterations in the expression of additional molecular markers for each of these two types of cardioblasts, such as the novel T-box-containing gene Tb66F2 and the potassium channel-encoding gene sur. These observations suggest that seven-up has a role in diversifying cardioblast identities within each segment. We also describe the tinman cis sequences that mediate tinman repression by seven-up and examine whether Seven-up can bind these sequences to directly inhibit tinman.