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Hua, X.

Publications and source records attributed to Hua, X..

3 recordsLinked to original sources

The ecological drivers of variation in global language diversity

Language diversity is distributed unevenly over the globe. Why do some areas have so many different languages and other areas so few? Intriguingly, patterns of language diversity resemble biodiversity patterns, leading to suggestions that similar mechanisms may underlie both linguistic and biological diversification. Here we present the first global analysis of language diversity that identifies the relative importance of two key ecological mechanisms suggested to promote language diversification - isolation and ecological risk - after correcting for spatial autocorrelation and phylogenetic non-independence. We find significant effects of climate on language diversity consistent with the ecological risk hypothesis that areas of high year-round productivity lead to more languages by supporting human cultural groups with smaller distributions. Climate has a much stronger effect on language diversity than landscape features that might contribute to isolation of cultural groups, such as altitudinal variation, river density, or landscape roughness. The association between biodiversity and language diversity appears to be an incidental effect of their covariation with climate, rather than a causal link between the two. While climate and landscape provide strong explanatory signal for variation in language diversity, we identify a number of areas of high unexplained language diversity, with more languages than would be predicted from environmental features alone; notably New Guinea, the Himalayan foothills, West Africa, and Mesoamerica. Additional processes may be at play in generating higher than expected language diversity in these regions.

ecology

Interaction of BIR2/3 of XIAP with E2F1/Sp1 Activates MMP2 and Bladder Cancer Invasion by Inhibiting Src Translation

Although X-linked inhibitor of apoptosis protein (XIAP) is associated with cancer cell behaviors, the structure-based function of XIAP in promotion human bladder cancer (BC) invasion is barely explored. Herein, we discovered that ectopic expression of the BIR domains of XIAP rescued the MMP2 activation and invasion in XIAP-deleted BC cells, while Src was further defined as a XIAP downstream negative regulator for MMP2 activation and BC invasion. The inhibition of Src expression by BIR domains was caused by attenuation of Src protein translation upon miR-203 upregulation resulting from direct interaction of BIR2 and BIR3 with E2F1 and Sp1, consequently leading to fully activation of E2F1/Sp1. Our findings provide a novel insight into understanding of specific function of BIR2 and BIR3 of XIAP in BC invasion, which will be highly significant for the design/synthesis of new BIR2/BIR3-based compounds for invasive BC treatment.

cancer biology

Specific miRNA-GPCR networks regulate Sox9a/Sox9b activities to promote gonadal renewal in zebrafish

Fertility and endocrine function rely on a tightly regulated synchronicity within the hypothalamic-pituitary gonadal (HPG) axis. FSH/cAMP/MAPK/ Sox9 axis signaling and its regulated specific miRNAs are thought to regulate vertebrate gonadal development and sex differentiation, and yet the regulatory networks are largely unknown. Here we construct small RNA and mRNA libraries from sexually matured ovary and testis of zebrafish to identify specific miRNA-target pairs. Integration of Targetscan prediction and in vivo induced gene expression highlight four specific miRNAs that conditionally target three G protein-coupled receptor (GPCR) x-Sox9 signaling genes, and implicate two regulatory circuits of miR430a-Sox9a in the testis and miR218a-Sox9b in the ovary. Co-injected Sox9a-miR430a mixture increases the proportion of spermatogonia but degenerates primary oocyte, while Sox9b-miR218a mixture induces renewal of ovarian follicles. Co-immunoprecipitation and mass-spectrometry analyses further reveal that miR430a and Sox9a synergistically activate testicular PKC/Rock1 signals while miR218a and Sox9b constrict ovary PKC/PI3K/Rock1 signaling. These results clarify specific miRNAs-GPCR regulatory networks of Sox9a/Sox9b switch, and also provide mechanistic insight into gonadal rejuvenation and plasticity.

developmental biology