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Chen, c.

Publications and source records attributed to Chen, c..

2 recordsLinked to original sources

Exploring genetic, expression and regulatory patterns of parental alleles in Muscovy duck (Cairina moschata) using haplotype-resolved assemblies

BackgroundAlthough the biological mechanism for heterosis has been debated for a long time, heterosis is widely utilized to increase the global productivity of crops and livestock. Recently, the mechanism has been well characterized in crops and livestock with a male-heterogametic XY system due to genomic assembly advancements, especially the availability of haploid genomes. However, the biological mechanism for heterosis remains unclear in poultry possessing the female-heterogametic ZW system. ResultsHere, we assembled chromosome-level diploid and haploid genomes of the Muscovy duck. We developed an efficient and cost-effective method to assemble 12 variation graph-haploid Muscovy duck genomes from three full-sibling pairs with high quality using short-read Illumina sequences. We further characterized genetic, expression and regulatory patterns of parental alleles at multiple scales. We found that maternal haploid genomes generally had more open chromatin organization and higher accessibility, and higher levels of gene expression, while showing similar DNA methylation levels when compared to paternal haploid genomes. In contrast, the female paternal Z chromosome showed the most, and the male paternal Z chromosome presented more, relaxed chromatin organization and chromatin accessibility, and gene expression compared to the male maternal Z chromosome. Thus, the ZW system largely relies on compensation and balance to regulate gene expression on the sex Z chromosome. Moreover, we identified non-Mendelian regions covering 0.26% of the genome ([~]3.18 Mb). These regions contained lower gene density, GC content, and repeat sequence frequency, but were enriched for DNA motifs bound by transcription factors, likely leading to a compacted chromatin structure and lower chromatin accessibility. ConclusionsOur work here provides a comprehensive profile of parental alleles genetic, expression and regulatory patterns in the female-heterogametic ZW system, and might be useful for the utilization of heterosis in poultry.

genomics↗

Activation of IP10/CXCR3 signaling with highly coincidental with PrPSc deposit in the brains of scrapie infected mice

Activation of chemokine IP10, also named as CXCL10, and its receptor CXCR3 in CNS is described in some neurodegenerative diseases. Our previous study has also demonstrated an increased brain IP10 levels in several scrapie infected rodent models. However, the detailed alteration of IP10/CXCR3 signaling in CNS during prion infection remains unsettled. Here, we found the increased IP10 signals in the brains of scrapie infected mice mainly localized in the neurons and the activated microglia using various methodologies. The levels of CXCR3 were markedly increased in brains of the scrapie infected mice and in the prion infected cell line SMB-S15. The increased CXCR3 mainly distributed in neurons. Obviously morphological colocalizations of PrP/PrPSc with IP10 and CXCR3 in the brains of scrapie infected mice were observed in the assays of immunohistochemistry (IHC) and immunofluorescence. Additionally, IHC analysis with whole brain sections demonstrated that the increased IP10 and CXCR3 accumulated in the brain regions with more PrPSc deposits. Co-immunoprecipitation and biomolecular interaction assays identified the evidence for the molecular interactions of PrP with IP10 and CXCR3. Compared to the normal partner cell line SMB-PS, the more portion of IP10 accumulated insides of prion infected SMB-S15 cells. Removal of prion replication in SMB-S15 cells by resveratrol converted the pattern of the accumulation and secretion of cellular IP10. Our data here demonstrate an activation of IP10/CXCR3 signaling in the brain tissues of prion infection, highly coincidental with PrPSc deposit. Modulation of brain IP10/CXCR3 signaling is potential therapeutic target for reducing the progression of prion diseases.

neuroscience↗