3 research outputs found

    KRAB zinc finger protein ZNF676 controls the transcriptional influence of LTR12-related endogenous retrovirus sequences.

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    BACKGROUND: Transposable element-embedded regulatory sequences (TEeRS) and their KRAB-containing zinc finger protein (KZFP) controllers are increasingly recognized as modulators of gene expression. We aim to characterize the contribution of this system to gene regulation in early human development and germ cells. RESULTS: Here, after studying genes driven by the long terminal repeat (LTR) of endogenous retroviruses, we identify the ape-restricted ZNF676 as the sequence-specific repressor of a subset of contemporary LTR12 integrants responsible for a large fraction of transpochimeric gene transcripts (TcGTs) generated during human early embryogenesis. We go on to reveal that the binding of this KZFP correlates with the epigenetic marking of these TEeRS in the germline, and is crucial to the control of genes involved in ciliogenesis/flagellogenesis, a biological process that dates back to the last common ancestor of eukaryotes. CONCLUSION: These results illustrate how KZFPs and their TE targets contribute to the evolutionary turnover of transcription networks and participate in the transgenerational inheritance of epigenetic traits

    Cellular advective-diffusion drives the emergence of bacterial surface colonization patterns and heterogeneity

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    Microorganisms navigate and divide on surfaces to form multicellular structures called biofilms, the most widespread survival strategy found in the bacterial world. One common assumption is that cellular components guide the spatial architecture and arrangement of multiple species in a biofilm. However, bacteria must contend with mechanical forces generated through contact with surfaces and under fluid flow, whose contributions to colonization patterns are poorly understood. Here, we show how the balance between motility and flow promotes the emergence of morphological patterns in Caulobacter crescentus biofilms. By modeling transport of single cells by flow and Brownian-like swimming, we show that the emergence of these patterns is guided by an effective Peclet number. By analogy with transport phenomena we show that, counter-intuitively, fluid flow represses mixing of distinct clonal lineages, thereby affecting the interaction landscapes between biofilm-dwelling bacteria. This demonstrates that hydrodynamics influence species interaction and evolution within surface-associated communities

    Biofilms deform soft surfaces and disrupt epithelia

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    During chronic infections and in microbiota, bacteria predominantly colonize their hosts as multicellular structures called biofilms. A common assumption is that biofilms exclusively interact with their hosts biochemically. However, the contributions of mechanics, while being central to the process of biofilm formation, have been overlooked as a factor influencing host physiology. Specifically, how biofilms form on soft, tissue-like materials remains unknown. Here, we show that biofilms of the pathogens Vibrio cholerae and Pseudomonas aeruginosa can induce large deformations of soft synthetic hydrogels. Biofilms buildup internal mechanical stress as single cells grow within the elastic matrix. By combining mechanical measurements and mutations in matrix components, we found that biofilms deform by buckling, and that adhesion transmits these forces to their substrates. Finally, we demonstrate that V. cholerae biofilms can generate sufficient mechanical stress to deform and even disrupt soft epithelial cell monolayers, suggesting a mechanical mode of infection
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