Foxj1 regulates asymmetric gene expression during left–right axis patterning in mice

Zhang, Min; Bolfing, Mary F.; Knowles, Heather; Karnes, Hope; Hackett, Brian P.

doi:10.1016/j.bbrc.2004.09.207

Cited by 34 publications

(32 citation statements)

References 48 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…−/− embryos, consistent with the randomization of LR patterning cues (Zhang et al, 2004). In one Foxj1 −/− embryo, both left and right walls of the straightened stomach are highly polarized (Fig.…”

Section: Fig 3adg) This Lr Asymmetric Tissue Architecture Is Varisupporting

confidence: 75%

Stomach curvature is generated by left-right asymmetric gut morphogenesis

et al. 2017

View full text Add to dashboard Cite

Left-right (LR) asymmetry is a fundamental feature of internal anatomy, yet the emergence of morphological asymmetry remains one of the least understood phases of organogenesis. Asymmetric rotation of the intestine is directed by forces outside the gut, but the morphogenetic events that generate anatomical asymmetry in other regions of the digestive tract remain unknown. Here, we show in mouse and Xenopus that the mechanisms that drive the curvature of the stomach are intrinsic to the gut tube itself. The left wall of the primitive stomach expands more than the right wall, as the left epithelium becomes more polarized and undergoes radial rearrangement. These asymmetries exist across several species, and are dependent on LR patterning genes, including Foxj1, Nodal and Pitx2. Our findings have implications for how LR patterning manifests distinct types of morphological asymmetries in different contexts.

show abstract

Section: Fig 3adg) This Lr Asymmetric Tissue Architecture Is Varisupporting

confidence: 75%

Stomach curvature is generated by left-right asymmetric gut morphogenesis

et al. 2017

View full text Add to dashboard Cite

show abstract

“…C2, H1, J1, P1, and P4. [15][16][17][18] Four of these 6 factors were identified as candidate regulators of pathological hypertrophy in humans by our analysis ( Figure 6B). In particular, loss of FOXP1 results in defective cardiomyocyte proliferation and differentiation.…”

Section: Discussionmentioning

confidence: 90%

“…14 Many FOX factors are critical regulators of tissue-specific gene expression and morphogenesis, including cardiovascular development. [15][16][17][18][19] To identify candidate FOX factors associated with heart failure, we determined which FOX factors were present in human myocardium. On the basis of microarray data, a minimum of 15 FOX factors were present in left ventricular myocardium at levels comparable to those of established hypertrophic factors such as MEF2 ( Figure 6A).…”

Section: Fox Transcription Factors In Human Heart Failurementioning

confidence: 99%

Transcriptional Genomics Associates FOX Transcription Factors With Human Heart Failure

et al. 2006

View full text Add to dashboard Cite

Background-Specific transcription factors (TFs) modulate cardiac gene expression in murine models of heart failure, but their relevance in human subjects remains untested. We developed and applied a computational approach called transcriptional genomics to test the hypothesis that a discrete set of cardiac TFs is associated with human heart failure. Methods and Results-RNA isolates from failing (nϭ196) and nonfailing (nϭ16) human hearts were hybridized with Affymetrix HU133A arrays, and differentially expressed heart failure genes were determined. TF binding sites overrepresented in the Ϫ5-kb promoter sequences of these heart failure genes were then determined with the use of public genome sequence databases. Binding sites for TFs identified in murine heart failure models (MEF2, NKX, NF-AT, and GATA) were significantly overrepresented in promoters of human heart failure genes (PϽ0.002; false discovery rate 2% to 4%). In addition, binding sites for FOX TFs showed substantial overrepresentation in both advanced human and early murine heart failure (PϽ0.002 and false discovery rate Ͻ4% for each). A role for FOX TFs was supported further by expression of FOXC1, C2, P1, P4, and O1A in failing human cardiac myocytes at levels similar to established hypertrophic TFs and by abundant FOXP1 protein in failing human cardiac myocyte nuclei. Conclusions-Our results provide the first evidence that specific TFs identified in murine models (MEF2, NKX, NFAT, and GATA) are associated with human heart failure. Moreover, these data implicate specific members of the FOX family of TFs (FOXC1, C2, P1, P4, and O1A) not previously suggested in heart failure pathogenesis. These findings provide a crucial link between animal models and human disease and suggest a specific role for FOX signaling in modulating the hypertrophic response of the heart to stress in humans.

show abstract

“…In the early embryo, FOXJ1 regulates gene(s) controlling left-right asymmetry, such as Lrd (38). Lack of FOXJ1 results in the failure of cilia formation in the node, resulting in failure to express lefty-2 and the randomization of sites of Nodal and PITX2, proteins that control situs, in turn influencing lung lobulation (285). FOXJ1 also regulates IkB-␤, inhibiting NFB activation, thereby inhibiting inflammation during lung repair (128).…”

Section: A Differentiation Of Basal Cells (P63)mentioning

confidence: 99%

Transcriptional Control of Lung Morphogenesis

Maeda

Davé²,

Whitsett³

2007

Physiological Reviews

433

387

View full text Add to dashboard Cite

The vertebrate lung consists of multiple cell types that are derived primarily from endodermal and mesodermal compartments of the early embryo. The process of pulmonary organogenesis requires the generation of precise signaling centers that are linked to transcriptional programs that, in turn, regulate cell numbers, differentiation, and behavior, as branching morphogenesis and alveolarization proceed. This review summarizes knowledge regarding the expression and proposed roles of transcription factors influencing lung formation and function with particular focus on knowledge derived from the study of the mouse. A group of transcription factors active in the endodermally derived cells of the developing lung tubules, including thyroid transcription factor-1 (TTF-1), β-catenin, Forkhead orthologs (FOX), GATA, SOX, and ETS family members are required for normal lung morphogenesis and function. In contrast, a group of distinct proteins, including FOXF1, POD1, GLI, and HOX family members, play important roles in the developing lung mesenchyme, from which pulmonary vessels and bronchial smooth muscle develop. Lung formation is dependent on reciprocal signaling among cells of both endodermal and mesenchymal compartments that instruct transcriptional processes mediating lung formation and adaptation to breathing after birth.

show abstract

Foxj1 regulates asymmetric gene expression during left–right axis patterning in mice

Cited by 34 publications

References 48 publications

Stomach curvature is generated by left-right asymmetric gut morphogenesis

Stomach curvature is generated by left-right asymmetric gut morphogenesis

Transcriptional Genomics Associates FOX Transcription Factors With Human Heart Failure

Transcriptional Control of Lung Morphogenesis

Contact Info

Product

Resources

About