High impact information on Lfng

• These results indicate that Lfng encodes an essential component of the Notch signalling pathway during somitogenesis in mice [1].
• Here we show that mice homozygous for a targeted mutation of the lunatic fringe (Lfng) gene, one of the mouse homologues of fringe, have defects in somite formation and anterior-posterior patterning of the somites [1].
• Spatial comparison revealed that Hes7 and Lunatic fringe (Lfng) transcription occurs in the Hes7 protein-negative domains [2].
• A molecular oscillator that controls the expression of cyclic genes such as lunatic fringe (Lfng) in the presomitic mesoderm has been shown to be coupled with somite formation in vertebrate embryos [3].
• Lfng-null progenitors generated few thymocytes in competitive assays, whereas Lfng overexpression converted thymocytes into 'supercompetitors' with enhanced binding of Delta-like ligands and blocked T lymphopoiesis from normal progenitors [4].

Biological context of Lfng

• Our data are consistent with a model in which alternations of Lfng activity between ON and OFF states in the presomitic mesoderm prior to somite segmentation are critical for proper somite patterning, and suggest that Notch signaling might not be the only determinant of cyclic gene expression in the presomitic mesoderm of mouse embryos [3].
• To clarify whether Lfng influences airway cell differentiation, Lfng was overexpressed in distal epithelial cells of the developing mouse lung [5].
• A BAC contig was constructed from three BAC clones showing positive signals of Lfng and 11MMHAP75FRD8.seq near the Jsr locus on chromosome 5 [6].

Anatomical context of Lfng

• Here we demonstrate that a mutation in the Lfng gene partially suppresses the effects of the Jag2 mutation on hair cell development [7].
• Other components of the Notch pathway, including the Lunatic fringe (Lfng) gene, are also expressed during differentiation of the inner ear in mice [6] [7] [8] [9] [10] [7].
• In contrast to the Jag2 gene, which is expressed in hair cells, the Lfng gene is expressed in non-sensory supporting cells in the mouse cochlea [10] [7].
• In mice homozygous for targeted mutations of both Jag2 and Lfng, the generation of supernumerary hair cells in the inner hair cell row is suppressed, while supernumerary hair cells in the outer hair cell rows are unaffected [7].
• Here we show that developmental stage-specific expression of the glycosyltransferase lunatic fringe (Lfng) is required for coordination of the access of T cell progenitors to intrathymic niches that support Notch1-dependent phases of T cell development [4].

Associations of Lfng with chemical compounds

• Our results point to a Lfng-dependent role for Notch signalling in the development of nephron segments, especially the proximal tubules [8].

Regulatory relationships of Lfng

• These results are consistent with a model in which oscillatory Notch signaling underlies the segmentation clock and directly activates and indirectly represses Lfng expression [9].

Other interactions of Lfng

• Lfng-deficient mice and Dll3-deficient mice exhibit very similar defects, and marker analysis suggests that progression of the segmentation clock is disrupted in Dll3 mutants [10].
• Overexpression of Lfng did not affect spatial or temporal expression of Hes1 and Mash-1 [5].
• Neuroendocrine CGRP and protein gene product 9.5 expression was not altered by Lfng overexpression [5].
• Overexpression of Lfng had no effect on mesenchymal cell marker (alpha-sma, vWF, PECAM-1) expression [5].
• Expression pattern of Lfng in the PSM of Jsr-mutant embryos was similar to that of the normal (C57BL/6) embryos [11].

Analytical, diagnostic and therapeutic context of Lfng

• Lfng was identified as the candidate gene for Jsr, but sequence analysis of this gene revealed no substitution in the coding region of cDNA [6].

References