Determination of left-right asymmetric expression of nodal (ital) by a left side-specific enhancer with sequence similarity to a lefty-2 (ital) enhancer

Article Abstract:

Similar transcription mechanisms seem to be behind asymmetric expression of nodal (ital), a gene expressed on the left side of developing mouse embryos and implicated in left/right (L/R) axis formation, and also of lefty-2 (ital) and of the expression earlier of nodal (ital) in endoderm and epiblasts. The transcriptional regulatory element of nodal responsible for the asymmetric expression of the gene has been identified. Intron 1 contains a left side-specific enhancer (ASE) that can direct transgene expression in the lateral plate mesoderm and prospective floor plate on the left.

Vertebrates, Genetic regulation, Mice, mutant strains, Mutant mice, Embryology, Experimental, Embryological research

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lefty-1 is required for left-right determination as a regulator of lefty-2 and nodal

Article Abstract:

Developing mice deficient in the gene lefty-1 are monitored to investigate the function of this gene in the development of laterality. Results reveal that mice lacking this gene developed left-to-right positional anomalies in the visceral organs. The most prominent of these positional defects was thoracic left isomerism. Further, the absence of lefty-1 resulted in the bilateral expression of nodal, lefty-2 and Pitx2, the expression of which is normally limited to the left. It is concluded that lefty-1 restricts the expression of these genes on the left side of the embryo.

Laterality

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Distinct transcriptional regulatory mechanisms underlie left-right asymmetric expression of lefty-1 and lefty-2

Article Abstract:

Studies show that different regulatory mechanisms are responsible for lefty-1 and lefty-2 gene expression in mice embryos. Despite their similarities, the two genes are expressed through a left side-specific enhancer for lefty-2 and a combination of a right side-specific silencer and bilateral enhancers for lefty-1. These processes account for their asymmetric expression.

Reports, Developmental genetics

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