bioRxiv Science⌕ Search

Biology subjects

Liang, Y.-Y.

Publications and source records attributed to Liang, Y.-Y..

2 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↗

EZH2/ hSULF1 axis mediates receptor tyrosine kinase signaling to shape cartilage tumor progression

BackgroundChondrosarcomas are primary cancers of cartilaginous tissue and capable of alteration to highly aggressive, metastatic, and treatment-refractory states, leading to a poor prognosis with a five-year survival rate at 11 months for the dedifferentiated subtype. At present, the surgical resection of chondrosarcoma is the only effective treatment, and no other treatment options including targeted therapies, conventional chemotherapies, or immunotherapies are available for these patients. MethodsA non-biased ChIP sequence, cDNA microarray analysis, and validation of chondrosarcoma cell lines identified sulfatase 1(SULF1) as the top EZH2-targeted gene to regulate chondrosarcoma progression. Receptor tyrosine kinase (RTK) array of chondrosarcoma cells with vector control or ectopically expressed SULF1 revealed that cMET was the downstream signal. The regulation of the EZH2/SULF1/cMET axis was further validated in mice and patient samples with mice models and chondrosarcoma tissue array, respectively. ResultsThe EZH2/SULF1/cMET axis is identified, which contributes to the malignancy of chondrosarcoma and provides a potential therapeutic option for the disease. Ectopically expressed SULF1 or pharmaceutical inhibition of the cMET pathway significantly retards the chondrosarcoma growth and extends mice survival. ConclusionsThe results not only established a signal pathway promoting the malignancy of chondrosarcoma but also provided a therapeutic potential for further development of effective target therapy to treat chondrosarcoma.

cancer biology↗