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An endogenous retrovirus-derived long non-coding RNA promotes fetal cardiomyocyte migration in primates

ABSTRACT: The protein-coding gene networks regulating heart development are well known. Less understood are the roles of long non-coding RNAs (lncRNAs), many of which are poorly conserved due to their origins from transposable elements (TEs) such as endogenous retroviruses (ERVs). Here, we report hundreds of ERV elements from the primate-specific MER41 family are expressed in pluripotent cell-derived cardiomyocytes and fetal heart, some of which are regulated by the cardiogenic transcription factor TBX5. The most significant of these are located within BANCR, an lncRNA exclusively expressed in primate fetal cardiomyocytes in normal physiology. Surprisingly, BANCR promotes cellular movement in fetal cardiomyocytes, which is due in part to Rho GTPase and ephrin receptor signaling. We postulate that ERV-derived BANCR is a recent evolutionary mechanism for enabling larger heart sizes in primates, and underscores the remarkable retroviral origins of humans.

ORGANISM(S): Gorilla gorilla Mus musculus Pan troglodytes Homo sapiens Macaca mulatta

PROVIDER: GSE111930 | GEO | 2020/08/11

REPOSITORIES: GEO

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Project description:Background: Prion diseases such as bovine spongiform encephalopathies (BSE) are transmissible neurodegenerative diseases which are presumably caused by an infectious conformational isoform of the cellular prion protein. Previous work has provided evidence that in murine prion disease the endogenous retrovirus (ERV) expression is altered in the brain. To determine if prion-induced changes in ERV expression are a general phenomenon we used a non-human primate model for prion disease. Results: Cynomolgus macaques (Macaca fasicularis) were infected intracerebrally with BSE-positive brain stem material from cattle and allowed to develop prion disease. Brain tissue from the basis pontis and vermis cerebelli of the six animals and the same regions from four healthy controls were subjected to ERV expression profiling using a retrovirus-specific microarray and quantitative real-time PCR. We could show that Class I gammaretroviruses HERV-E4-1, ERV-9, and MacERV-4 increase expression in BSE-infected macaques. In a second approach, we analysed ERV-K-(HML-2) RNA and protein expression in extracts from the same cynomolgus macaques. Here we found a significant downregulation of both, the macaque ERV-K-(HML-2) Gag protein and RNA in the frontal/parietal cortex of BSE-infected macaques. Conclusions: We provide evidence that dysregulation of ERVs in response to BSE-infection can be detected on both, the RNA and the protein level. To our knowledge, this is the first report on the differential expression of ERV-derived structural proteins in prion disorders. Our findings suggest that endogenous retroviruses may induce or exacerbate the pathological consequences of prion-associated neurodegeneration. Cynomolgus macaques (Macaca fasicularis) were infected intracerebrally with BSE-positive brain stem material from cattle and allowed to develop prion disease. Brain tissue from the basis pontis and vermis cerebelli of the six animals and the same regions from four healthy controls were subjected to ERV expression profiling using a retrovirus-specific microarray and quantitative real-time PCR. In a second approach, ERV-K-(HML-2) RNA and protein expression was analysed in extracts from the same cynomolgus macaques.

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An endogenous retrovirus-derived long non-coding RNA promotes fetal cardiomyocyte migration in primates

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