Expression patterns of Id1, Id2, and Id3 are highly related but distinct from that of Id4 during mouse embryogenesis

Abstract

The murine dominant negative helix-loop-helix (dnHLH) proteins inhibit the activities of bHLH transcription factors in diverse cell lineages (Benezra et al. . Currently, there are four members in the dnHLH family, Idl, Id2, Id3, and Id4. In this report, we have performed a detailed comparative in situ hybridization analysis to examine their expression pattern during post-gastrulational mouse development. Idl, 2, and 3 are expressed in multiple tissues, whereas Id4 expression can only be detected in neuronal tissues and in the ventral portion of the epithelium of the developing stomach. The regions where I d 1 3 genes are expressed, such as gut, lung, kidney, tooth, whisker, and several glandular structures, are undergoing active morphogenetic activities. The expression patterns of Idl, 2, and 3 overlap in many organs, except in the tissues derived from primitive gut. In the latter, Id1 and Id3 signals are detected in the mesenchyme surrounding the epithelium, whereas Id2 is expressed within the epithelium. The difference in the patterns of expressions of I d 1 3 and Id4 suggest that the dominant negative transcriptional activity of these two subclasses of the Id family may have different physiological consequences. o 1996 Witey-Liss, Inc.

Expression of Id2 in the second heart field and cardiac defects in Id2 knock‐out mice

“…The role of Id2 in heart development (Jen et al, 1996;Fraidenraich et al, 2004) and cardiac conduction system development (Moskowitz et al, 2007) has been previously recognized, but detailed reports on expression patterns of Id2 in the heart, specifically at the venous pole and proximal cardiac conduction system in subsequent embryonic stages, are lacking. Key findings in the current study are (1) the expression of Id2 in cardiac progenitor cells not only at the arterial but also at the venous pole of the heart, including the area of the putative SAN; (2) a severe cardiac phenotype in Id2 knockout embryos with abnormal drainage patterns at the arterial pole (double outlet right ventricle) as well as at the venous pole (abnormal level of drainage of systemic and pulmonary veins) of the heart; (3) congenital heart malformations related to anterior and posterior second heart field deficiency in Id2 knockout embryos.…”

“…Id-genes negatively regulate basic helix-loophelix proteins. bHLH proteins with (partially) overlapping expression pattern with Id-genes include E2A, M-twist, paraxis, Screraxis, and Hes1 (Jen et al, 1996;Bai et al, 2007;Jogi et al, 2002). For many of these genes, a functional pathway in heart development has not been shown yet.…”

“…They promote cell proliferation, have a possible role in control of cell differentiation and cell lineage commitment, and keep cells in an undifferentiated state (Lim et al, 2008;Yokota et al, 2001). Four Id family members, Id1-4, have been isolated in chick and mouse (Jen et al, 1996;Martinsen et al, 2004). Id2 is involved in many developmental processes including: myogenesis, neurogenesis, cell growth, and cell fate specification (Yokota et al, 2001).…”

“…Overlapping expression patterns during development of these 3 Id genes have been described in the endocardial cushions and mesenchyme of the outflow tract, whereas expression of Id4 was not found in cardiac tissues with in situ hybridization analysis (Jen et al, 1996). To date, a detailed comparison of cardiac expression patterns of the Id-genes is not available.…”

“…To date, a detailed comparison of cardiac expression patterns of the Id-genes is not available. In the heart, Id2 expression was described in the endocardial cushions of the atrioventricular canal and the outflow tract, the cardiac valves, the epicardium and endocardium, but not the working myocardium (Fraidenraich et al, 2004;Jen et al, 1996). Ablation of two Id-genes in any combination from Id1, 2, or 3 results in severe cardiac defects including ventricular septal defects, thinning of the myocardium, and hypoplastic cushions in the atrioventricular canal and outflow tract (Fraidenraich et al, 2004).…”