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Articles by X Nie
Total Records ( 3 ) for X Nie
  X Mao , X Nie , F Cao and J. Chen

Here we reported that, in Saccharomyces cerevisiae, deleting Swi1 (ScSwi1), a core component in Swi/Snf complex, caused defects of invasive growth, pseudohyphal growth, FLO11 expression, and proper cell separation. Re-introduction of SWI1 into the swi1 mutants could suppress all defects observed. We also showed that overproducing Swi1 could suppress the defect of flo8 cells in pseudohyphal growth in diploids, but not invasive growth in haploids. Overexpression of SWI1 could not bypass the requirement of Ste12 or Tec1 in invasive growth or pseudohyphal growth. We concluded that the Swi/Snf complex was required for FLO11 expression and proper cell separation, and both the FLO8 and STE12 genes should be present for the complex to function for the invasive growth but only the STE12 gene was required for the pseudohyphal growth. Ectopic expression of Candida albicans SWI1 (CaSWI1) could partially complement the defects examined of haploid Scswi1 mutants, but failed to complement the defects examined of diploid Scswi1/Scswi1 mutants. Overexpressing CaSwi1 mitigated invasive and pseudohyphal growth defects resulting from deletions in the MAP kinase and cAMP pathways. The integrity of S. cerevisiae Swi/Snf complex is required for invasive and filamentous growth promoted by overexpressing CaSwi1.

  X Nie , X Liu , H Wang and J. Chen

Phenotypic switching in Candida albicans spontaneously generates different cellular morphologies. The reversible switching between white and opaque phenotypes is regulated by multiple regulators including Efg1 and Wor1. In mating-type-like locus (MTL) homozygous cells, the Efg1 functions as a repressor, whereas the Wor1 acts as an activator in white–opaque switching. We presented evidence that switching between white and opaque in efg1/efg1 mutant is regulated by ambient pH. In pH 6.8 media, the efg1/efg1 mutant cells exhibited opaque form, but shifted to white form in pH 4.5 media. The pH-dependent morphological switching is not blocked by further deletion of WOR1 in the efg1/efg1 mutant. Correlated with the phenotype, the opaque-phase-specific gene OP4 was induced in efg1/efg1 mutant cells when cultured in pH 6.8 media, and was repressed in pH 4.5 media. Consistently, the MTLa efg1/efg1 mutant cells could mate efficiently with MTL cells in pH 6.8 media, but poorly in pH 4.5 media. Ectopic expression of the Rim101-405 allele in the efg1/efg1 mutant helped to bypass the pH restriction on white–opaque switching and show opaque form in both neutral and acidic media. We proposed that relief of the Efg1 repression enables C. albicans to undergo white–opaque switching in pH-dependent regulation mediated by Rim101-signaling pathway.

  Y Wang , D Liang , S Wang , Z Qiu , X Chu , S Chen , L Li , X Nie , R Zhang , Z Wang and D. Zhu

It has been previously reported by us that hypoxia activates lung 15-lipoxygenase (15-LO), which catalyzes arachidonic acid to 15-hydroxyeicosatetraenoic acid (15-HETE), leading to the constriction of pulmonary artery (PA). Rho-associated serine/threonine kinase (ROK), a downstream effector of small GTPase RhoA that may be modulated by G-protein and tyrosine kinase, plays an important role in smooth muscle contraction. However, whether the 15-HETE induced PA vasoconstriction involves the Rho/ROK pathway remains to be demonstrated. Therefore, we studied the contribution of ROK as well as G-protein and tyrosine kinase to the 15-HETE induced pulmonary vasoconstriction using PA ring technique, RNA interference technology, RP-HPLC, western blot and RT-PCR combined with the blockers. The hypoxia-induced expression of ROK is regulated by 15-HETE in rat PA smooth muscle cells (PASMCs), leading to vasoconstriction. The up-regulation of ROK expression caused by 15-HETE appears to be mediated by the G-protein and tyrosine kinase pathways. The translocation of ROK2 from the nucleus to the cytoplasm during hypoxia exposure relies on the mechanism for 15-HETE production. These results suggest that 15-HETE may mediate the up-regulation of ROK expression through G-protein and tyrosine kinase pathways under hypoxic condition, leading to PA vasoconstriction.

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