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Lysine Degradation Reprograms Tumour Immunity through Histone Crotonylation [RNA-seq]

ABSTRACT: To understand how GCDH enhances the oncogenic traits in GSCs, we carried out comparative transcriptomic analysis in two patient-derived GSCs (GSC23, GSC3028) with or without GCDH depletion to identify the driving events. To further examine the connection between lysine catabolism and GSC functions, we controlled L-lysine culture concentrations (0.2 and 2 mM) of GSCs in lysine-deprived media and performed RNA-seq. To address the functional significance of ECHS1 loss in tumour biology, we carried out RNA-seq in two early-passage DGCs (DGC23, DGC3028) with or without ECHS1 depletion. Kcr, H3K27ac or H3K9me3 ChIP-seq was performed in GSC23 to understand the molecular basis of how GCDH loss or lysine restriction affects chromatin landscape.

ORGANISM(S): Homo sapiens

PROVIDER: GSE208616 | GEO | 2023/03/16

REPOSITORIES: GEO

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Lysine Degradation Reprograms Tumour Immunity through Histone Crotonylation [ChIP-seq]

Project description:To understand how GCDH enhances the oncogenic traits in GSCs, we carried out comparative transcriptomic analysis in two patient-derived GSCs (GSC23, GSC3028) with or without GCDH depletion to identify the driving events. To further examine the connection between lysine catabolism and GSC functions, we controlled L-lysine culture concentrations (0.2 and 2 mM) of GSCs in lysine-deprived media and performed RNA-seq. To address the functional significance of ECHS1 loss in tumour biology, we carried out RNA-seq in two early-passage DGCs (DGC23, DGC3028) with or without ECHS1 depletion. Kcr, H3K27ac or H3K9me3 ChIP-seq was performed in GSC23 to understand the molecular basis of how GCDH loss or lysine restriction affects chromatin landscape.

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Identification of 67 histone marks and histone lysine crotonylation as a new type of histone modification

Project description:We report the identification of 67 previously undescribed histone modifications, increasing the current number of known histone marks by about 70%. We further investigated one of the marks, lysine crotonylation (Kcr), confirming that it represents an evolutionarily-conserved histone posttranslational modification. The unique structure and genomic localization of histone Kcr suggest that it is mechanistically and functionally different from histone lysine acetylation (Kac). Specifically, in both human somatic and mouse male germ cell genomes, histone Kcr marks either active promoters or potential enhancers. In male germinal cells immediately following meiosis, Kcr is enriched on sex chromosomes and specifically marks testis-specific genes, including a significant proportion of X-linked genes that escape sex chromosome inactivation in haploid cells. These results therefore dramatically extend the repertoire of histone PTM sites and designate Kcr as a specific mark of active sex chromosome-linked genes in postmeiotic male germ cells. 2 histone marks (pan-lysine acetylation and pan-lysine crotonylation) were studied in 1 human cell type and 2 mouse cell types using ChIP-Seq. Input was sequenced for each cell type as a control. Pan-anti_Kac and pan-anti_Kcr antibodies were custom developed with PTM BioLab, Co., Ltd (Chicago, IL).

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