Towards Understanding the Gene-Specific Roles of GATA Factors in Heart Development : Does GATA4 Lead the Way?

Funding: This work is supported by the British Heart Foundation (BHF): programme grant number: RG/18/8/33673 to Professor Stefan Hoppler. Acknowledgments: I would like to thank Stefan Hoppler for providing critical comments as well as valuable and constructive suggestions for the manuscript.Peer reviewedPublisher PD

Genome-wide transcriptomics analysis identifies sox7 and sox18 as specifically regulated by gata4 in cardiomyogenesis

This work was supported by British Heart Foundation (BHF Project Grant no PG/13/23/30080 to B.A.A and S.H.), Biotechnology and Biological Sciences Research Council (BB/M001695/1 to S.H.) and the University of Aberdeen (for A.T.L). Acknowledgements We’re grateful to Ms Yvonne Turnbull and Ms Kate Watt for technical assistance and lab management. We would like to thank Professor Cedric Blanpain and Dr Xionghui Li from Université Libre de Bruxelles for providing training of ES cell manipulation and Mesp1/Gata4 cell lines. We are grateful to Professor Todd Evans from Weill Cornell Medical College for generously providing iGata ES cell lines. We also would like to thank Professor Aaron Zorn and Scott Rankin for providing Xsox18 plasmid.Peer reviewedPublisher PD

Genome-wide transcriptomics analysis of genes regulated by GATA4, 5 and 6 during cardiomyogenesis in Xenopus laevis

Funding sources This work was supported by British Heart Foundation (BHF Project Grant no PG/13/23/30080 to B.A.A and S.H.), Biotechnology and Biological Sciences Research Council (BB/M001695/1 to S.H.) and the University of Aberdeen (for A.T.L).Peer reviewedPublisher PD

Foxh1/Nodal Defines Context-Specific Direct Maternal Wnt/β-Catenin Target Gene Regulation in Early Development

We thank Jessica Cheung (UC Irvine) and Yvonne Turnbull (University of Aberdeen) for technical and management support; Gert Jan Veenstra (Radboud University, Nijmegen) for discussion; and Adam Lynch and Victor Velecela (University of Aberdeen), for comments on the manuscript. We also thank Professor Masanori Taira (University of Tokyo, currently Chuo University) and Dr Norihiro Sudou (Nara Institute of Science and Technology, currently Tokyo Women's Medical University) for the siamois antibody; and Professor Dan Kessler (University of Pennsylvania) for siamois constructs. This research was supported by the Biotechnology and Biological Sciences Research Council (BBSRC) in the United Kingdom (BB/M001695/1) and by NIH in the United States (NIH GM126395). SH additionally acknowledges personal funding support as a Royal Society/Leverhulme Trust Senior Research Fellow (SRF\R1\191017).Peer reviewedPublisher PD

The Republican Journal: Vol. 93, No. 8 - February 24,1921

https://digitalmaine.com/rj_1921/1007/thumbnail.jp

Foxh1/Nodal Defines Context-Specific Direct Maternal Wnt/β-Catenin Target Gene Regulation in Early Development.

Although Wnt/β-catenin signaling is generally conserved and well understood, the regulatory mechanisms controlling context-specific direct Wnt target gene expression in development and disease are still unclear. The onset of zygotic gene transcription in early embryogenesis represents an ideal, accessible experimental system to investigate context-specific direct Wnt target gene regulation. We combine transcriptomics using RNA-seq with genome-wide β-catenin association using ChIP-seq to identify stage-specific direct Wnt target genes. We propose coherent feedforward regulation involving two distinct classes of direct maternal Wnt target genes, which differ both in expression and persistence of β-catenin association. We discover that genomic β-catenin association overlaps with Foxh1-associated regulatory sequences and demonstrate that direct maternal Wnt target gene expression requires Foxh1 function and Nodal/Tgfβ signaling. Our results support a new paradigm for direct Wnt target gene co-regulation with context-specific mechanisms that will inform future studies of embryonic development and more widely stem cell-mediated homeostasis and human disease