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Luo, W.-J.

Publications and source records attributed to Luo, W.-J..

4 recordsLinked to original sources

Evolutionary dynamics of the pan-centromere architecture in oaks

Centromeres ensure faithful chromosome segregation and genome stability, yet their DNA evolves rapidly, presenting a long-standing centromere paradox. Here we characterise the genomic and epigenomic architecture of >1,300 candidate centromeres from 111 high-quality Quercus (oak) genomes. We show that lineage-specific expansion of QuCEN146 satellite drives centromere turnover in oaks by displacing ancestral LTR-rich sequences into flanking regions, with genetic drift facilitating fixation of satellite-rich centromeres. Population-scale analyses in Q. serrata reveal extensive variation in satellite rich centromeres, generated by array expansion and contraction, strand-orientation shifts, and interspecific introgression. By contrast, LTR rich centromeres of Q. variabilis exhibit extremely low polymorphism and high collinearity across populations, sustained by suppressed local recombination, linked selection, and constrained LTR dynamics. We further demonstrate chromosome-independent evolutionary patterns for both satellite-rich and LTR-rich centromeres. Collectively, these findings demonstrate how evolutionary processes drive centromere turnover and shape contrasting centromeric sequence landscapes in forest trees.

evolutionary biology↗

Hsa_circ_0001304 promotes vascular smooth muscle cell autophagy and neointimal hyperplasia through the YTHDF2/mTOR axis

IntroductionAberrant autophagy in vascular smooth muscle cells (VSMCs) is associated with the progression of cardiovascular diseases. Recently, circular RNAs (circRNAs) have gradually been reported to regulate autophagy in VSMCs. ObjectivesThis study aims to investigate the role of hsa_circ_0001304 in VSMC autophagy and its underlying mechanism. MethodsThe combined use of dual-luciferase reporter gene assay, MeRIP-qRT-PCR, RIP-qRT-PCR, etc., was performed to verify the regulatory axis, hsa_circ_0001304/miR-636/YTHDF2/mTOR. Cell autophagy detection was performed to uncover the role of hsa_circ_0001304 on VSMC autophagy. The mouse carotid artery ligation model was conducted to assess the role of hsa_circ_0001304 on vascular neointimal hyperplasia. ResultsHsa_circ_0001304 acts as a sponge for miR-636, leading to an increase in the protein levels of YTHDF2. Subsequently, the YTHDF2 promotes the degradation of mTOR mRNA by binding to the latters m6A modification sites. Thus, by regulating the miR-636/YTHDF2/mTOR axis, hsa_circ_0001304 activates VSMC autophagy, aggravating neointimal hyperplasia. ConclusionOur findings suggest that autophagy-related hsa_circ_0001304 could serve as a novel therapeutic target for neointimal hyperplasia-related cardiovascular diseases. Including spacesOur study documents a novel VSMC autophagy-related circRNA, namely circ-1304, which activates VSMC autophagy through the miR-636/YTHDF2/mTOR axis, thereby exacerbating neointimal hyperplasia. Targeting autophagy-related circ-1304 may contribute to the treatment of neointimal hyperplasia-associated cardiovascular diseases.

molecular biology↗

HLJ1 amplifies endotoxin-induced sepsis severity by promoting IL-12 heterodimerization in macrophages

Heat shock protein (HSP) 40 has emerged as a key actor in both innate and adaptive immunity, whereas the role of HLJ1, a molecular chaperone in HSP40 family, in modulating endotoxin-induced sepsis severity is still unclear. Here, we use single-cell RNA sequencing to characterize mouse liver nonparenchymal cell populations under LPS (lipopolysaccharide) stimulation, and show that HLJ1 deletion affected IFN-{gamma}-related gene signatures in distinct immune cell clusters. HLJ1 deficiency also leads to reduced serum levels of IL-12 in LPS-treated mice, contributing to dampened production of IFN-{gamma} in natural killer cells but not CD4+ or CD8+ T cells, and subsequently to improved survival rate. Adoptive transfer of HLJ1-deleted macrophages into LPS-treated mice results in reduced IL-12 and IFN-{gamma} levels and protects the mice from IFN-{gamma}-dependent mortality. In the context of molecular mechanisms, HLJ1 is an LPS-inducible protein in macrophages and converts misfolded IL-12p35 homodimers to monomers, which maintains bioactive IL-12p70 heterodimerization and secretion. This study suggests HLJ1 causes IFN-{gamma}-dependent septic lethality by promoting IL-12 heterodimerization, and targeting HLJ1 has therapeutic potential in inflammatory diseases involving activating IL-12/IFN-{gamma} axis.

immunology↗

Empathic contagious pain and consolation in laboratory rodents: species and sex differences

Laboratory rodents are gregarious in nature and have a feeling of empathy when witnessing a familiar conspecific in pain. The rodent observers express two levels of empathic responses: observational contagious pain (OCP) and consolation. Here we examined the sex and species difference of OCP and consolation in male and female mice and rats. We observed no species difference in both OCP and consolation, but significant species difference in general social (allo-mouth and/or allo-tail sniffing) and non-social (self-grooming) behaviors. For sex difference, male mouse observers showed more allolicking and allogrooming behaviors toward a familiar conspecific in pain during and longer time increase in pain sensitivity after the PDSI than female mouse observers. However, no sex difference was observed in rats. Our results highlighted an evolutionary view of empathy that social animals including rodents also have the ability to feel, recognize, understand and share the others distressing states.

animal behavior and cognition↗