High impact information on H15

• Accordingly, loss of mid and H15 produces defects that mimic a wg gain-of-function phenotype [1].
• Furthermore, we show that loss of mid and H15 results in an anterior expansion of the expression of serrate (ser) in every segment, representing a second instance of target gene repression downstream of Hh signaling in the establishment of segment polarity [1].
• Taken together, the data suggest that nmr acts both in concert with and subsequent to pannier and tinman in cardiac specification and differentiation [2].
• Moreover, reducing nmr function in the absence of pannier further aggravates the deficit in cardiac mesoderm specification [2].
• Deletion mutants of nmr1 combined with mesoderm-specific knock-down of nmr2 exhibit phenotypes that suggest nmr is critical for correct specification of the cardiac progenitor populations as well as for morphogenesis and assembly of the contractile heart tube [2].

Biological context of H15

• Neuromancer Tbx20-related genes (H15/midline) promote cell fate specification and morphogenesis of the Drosophila heart [2].
• In addition, nmr mutants with less severe penetrance exhibit cell alignment defects of the myocardium at the dorsal midline, suggesting nmr is also required for cell polarity acquisition of the heart tube [2].
• We show that mid is among the earliest known genes that are specifically expressed in all cardioblasts during early embryogenesis, and H15 expression is subsequently activated in the same cells [3].

Other interactions of H15

• Comparison of the expression profiles of H15 and optomotor-blind to the Drosophila patterns suggests modifications also in the dorsal-ventral patterning system of the legs [4].

References