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Getting to the heart of the matter: Multispecies heart tissue proteome characterization

ABSTRACT: Structural birth defects are the leading cause of infant mortality in the US and Europe. Among these, congenital heart disease (CHD) is the most common. Historically, Xenopus, mouse, and pig have provided models for CHD. However, it remains unknown what proteins and pathways are conserved between these species and human. Furthermore, the proteome driving the differences between three-chambered (Xenopus) and four-chambered (mammalian) hearts is unknown. Comparative proteomics of heart tissue from species at different evolutionary points can reveal molecular processes underlying heart function. We examined heart tissue proteomes of Xenopus tropicalis, Xenopus laevis, Mus musculus, and Sus scrofa and assessed protein expression changes in the context of pathways and protein complexes, and enrichment of corresponding genes in human heart diseases.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Xenopus Laevis (african Clawed Frog) Xenopus Tropicalis Sus Scrofa Domesticus (domestic Pig) Mus Musculus (mouse)

TISSUE(S): Heart

SUBMITTER: Joel Federspiel

LAB HEAD: Ileana M Cristea

PROVIDER: PXD009577 | Pride | 2019-08-01

REPOSITORIES: Pride

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	20160719_PC139-Conlon_CD1-cyto_B4.raw	Raw
	20160719_PC139-Conlon_CD1-cyto_B5.raw	Raw
	20160720_PC139-Conlon_CD1-cyto_B1.raw	Raw
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	20160720_PC139-Conlon_CD1-cyto_B3.raw	Raw

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Publications

Distribution of T cell subsets and Langerhans cells in mycosis fungoides, and the effect of PUVA therapy.

Cox N H NH Turbitt M L ML Ashworth J J Mackie R M RM

Clinical and experimental dermatology 19861101 6

PMID: 3499264

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Project description:Genomic analyses of patients with congenital heart disease (CHD) have identified significant contribution from mutations affecting cilia genes and chromatin remodeling genes; however, the mechanism(s) connecting chromatin remodeling to CHD are unknown. Histone H2B mono-ubiquitination (H2Bub1) is catalyzed by the RNF20 complex consisting of RNF20, RNF40 and UBE2B. Here, we show significant enrichment of loss-of-function mutations affecting H2Bub1 in CHD patients (enrichment=6.01, p=1.67x10-03), some of whom had abnormal laterality associated with cilia dysfunction. In Xenopus, knockdown of rnf20 and rnf40 results in abnormal heart looping, defective development of left-right asymmetry and impaired cilia motility. Rnf20, Rnf40 and Ube2b affect LR patterning and cilia synergistically. Examination of global H2Bub1 level in Xenopus embryos shows that H2Bub1 is developmentally regulated and requires Rnf20. To examine gene-specific H2Bub1, we performed ChIP-seq of mouse ciliated and non-ciliated tissues and showed tissue-specific H2Bub1 marks significantly enriched at cilia genes including the transcription factor Rfx3. Rnf20 knockdown results in decreased levels of rfx3 mRNA in Xenopus, and exogenous rfx3 can rescue the Rnf20 depletion phenotype. These data suggest that Rnf20 functions at the Rfx3 locus regulating cilia motility and cardiac situs and identify H2Bub1 as an upstream transcriptional regulator controlling tissue-specific expression of cilia genes. Our findings mechanistically link the two functional gene ontologies that have been implicated in human CHD: chromatin remodeling and cilia function.

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Systems analysis of de novo mutations in congenital heart diseases identified a protein network in the hypoplastic left heart syndrome

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