High impact information on Foxl1

• The winged helix transcription factor Fkh6 is expressed in the mesoderm of the gastrointestinal tract directly adjacent to the endoderm-derived epithelium [1].
• Homozygous null mice for Fkh6 showed postnatal growth retardation secondary to severe structural abnormalities of the stomach, duodenum, and jejunum [1].
• Changes in the cellular phenotype and composition of the gastric and intestinal epithelia also suggests that epithelial cell-lineage allocation or differentiation may be affected by loss of Fkh6 [1].
• The fkh-6/MFH-1 locus maps close to the mouse mutation amputated, which is characterised by abnormal development of somitic and facial mesoderm [2].
• Foxl1 controls the Wnt/beta-catenin pathway by modulating the expression of proteoglycans in the gut [3].

Biological context of Foxl1

• Foxl1 is suggested to regulate the responsiveness of fetal intestinal mesenchymal cells to inductive signals mediated by Lymphotoxins during Peyer's patch organogenesis [4].
• To better understand the role of Foxl1 in epithelial morphogenesis, we examined the tissue structure and positioning of epithelial cells in the small intestine of Foxl1-deficient mice [5].
• Among the molecules involved in the membrane fusion event, only SNAP25 showed a significant decrease in mRNA expression, which likely caused the impairment in acid secretion from parietal cells in Foxl1-deficient mice, with the reduction in H+,K(+)-ATPase expression contributing to additional effect [6].

Anatomical context of Foxl1

• Foxl1 is a winged helix transcription factor expressed in the mesenchyme of the gastrointestinal tract [3].
• Foxl1 null mice display severe structural defects in the epithelia of the stomach, duodenum, and jejunum [3].
• In the small intestine of Foxl1-deficient mice, the formation of Peyer's patches is affected, particularly in the caudal region [4].
• The Foxl1 gene, which encodes a winged helix transcriptional regulator, is expressed in the mesenchymal layer of developing and mature gastrointestinal tract [4].
• Together, the data suggest that Foxl1 might be involved in cellular responses of gut-associated lymphoid tissues dependent upon the Lymphotoxins/Lymphotoxin beta-receptor axis [4].

Associations of Foxl1 with chemical compounds

• Consistent with these findings, Foxl1-/- mice show decreased levels of the intestinal D-glucose transporter SGLT1 [7].

Other interactions of Foxl1

• Reduction of SNAP25 in acid secretion defect of Foxl1-/- gastric parietal cells [6].
• We focused on the Wnt/beta-catenin signaling pathway as a possible target of Foxl1 as it has been shown to play a central role in gastrointestinal proliferation [3].

Analytical, diagnostic and therapeutic context of Foxl1

• Furthermore, real-time quantitative PCR indicated that a subset of Wnt family genes was highly expressed in the gut mesenchyme of Foxl1-deficient mice compared with that of wild-type mice [5].

References