DNMHMM: An approach to identify the differential nucleosome regions in multiple cell types based on a Hidden Markov Model

Xie, Jiahao; Cai, Yiran; Li, Huamei; Wu, Jiahui; Zhao, Xinlei; Luo, Kun; Sharma, Amit; Xie, Jingjing; Sun, Xiao; Liu, Hongde

doi:10.1016/j.biosystems.2019.104033

Cited by 3 publications

(1 citation statement)

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“…However, previously studies provided a hint that the genetic variants might engage in crosstalk with sequence-specific transcription factors and epigenetic patterns (including DNA methylation 30,31 ) thereby impacting the transcription of genes locally or remotely 32,33 . Importantly, each histone modification is unique to regulate the predictive chromatin signature at promoters, enhancer and TSS, still they can also share overlapping chromatin 34 signatures 35 . This is what we have observed in several SNP sites, where bivalent signature (co-existing “activating” and “silencing” nucleosomal modifications) poised to adopt either active or repressed chromatin states.…”

Section: Discussionmentioning

confidence: 99%

Common genetic variants associated with Parkinson’s disease display widespread signature of epigenetic plasticity

Sharma

Osato

Liu

et al. 2019

Sci Rep

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Parkinson disease (PD) is characterized by a pivotal progressive loss of substantia nigra dopaminergic neurons and aggregation of α-synuclein protein encoded by the SNCA gene. Genome-wide association studies identified almost 100 sequence variants linked to PD in SNCA. However, the consequences of this genetic variability are rather unclear. Herein, our analysis on selective single nucleotide polymorphisms (SNPs) which are highly associated with the PD susceptibility revealed that several SNP sites attribute to the nucleosomes and overlay with bivalent regions poised to adopt either active or repressed chromatin states. We also identified large number of transcription factor (TF) binding sites associated with these variants. In addition, we located two docking sites in the intron-1 methylation prone region of SNCA which are required for the putative interactions with DNMT1. Taken together, our analysis reflects an additional layer of epigenomic contribution for the regulation of the SNCA gene in PD.

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