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dc.contributor.authorIzquierdo-Bouldstridge, Andreaes_ES
dc.contributor.authorBustillos, Albertoes_ES
dc.contributor.authorBonet-Costa, Carleses_ES
dc.contributor.authorGarcía-Gomis, Danieles_ES
dc.contributor.authorJordan, Albertes_ES
dc.identifier.citationVIII Jornada de Cromatina i Epigenètica (2018)es_ES
dc.descriptionTrabajo presentado en la VIII Jornada de Cromatina i Epigenètica, organizada por la Secció de Biologia Molecular de la Societat Catalana de Biologia (SCB) y celebrada el 16 de marzo de 2018es_ES
dc.description.abstractSeven linker histone H1 variants exist in human somatic cells with distinct prevalence depending on the cell type and along differentiation. H1 bind to linker DNA contributing to higher order chromatin compaction. In addition, H1 seems to be actively involved in the regulation of gene expression. It is not well known whether the different variants have specific roles. We have shown that H1 variants are not distributed uniformly along the genome and there are differences between variants, H1.2 being the one showing the most specific pattern. We have explored functions of H1 variants by inducible shRNA-mediated knock-down of each of the variants. Knock-down of each H1 variant alters expression of a different, reduced subset of genes. Combined depletion of H1.2 and H1.4 has a strong deleterious effect in the cancer cells examined, and induces a strong interferon (IFN) response with up-regulation of many IFN-stimulated genes (ISGs). Although H1 participates to repress ISG promoters, its activation upon H1 KD is mainly generated by the expression of noncoding RNA generated from heterochromatic repeats including satellites. In conclusion, redundant H1-mediated silencing of heterochromatin is important to maintain genome stability and to avoid an unspecific growth-inhibiting IFN response.es_ES
dc.titleHistone H1 depletion triggers an interferon response in cancer cells via activation of heterochromatic repeatses_ES
dc.typepóster de congresoes_ES
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Appears in Collections:(IBMB) Comunicaciones congresos
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