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Mutations in AP22.65 Accelerate Flowering in Arabidopsis thaliana
Ji Hong Xing,Feng Ru Wang,Jiao Jia,Jing Zhang,Li Li,Zhan Chen,Qiao Yun Weng,Ping Yang,Ye Zhang,Bin Zhao,He Long Si,Jin Gao Dong,Jian Min Han 한국식물학회 2013 Journal of Plant Biology Vol.56 No.1
Identification of the gene(s) responsible for floweringtime in Arabidopsis has significant implications. We used theT-DNA insertion library of Arabidopsis thaliana to screen anearly-flowering mutant that exhibits accelerated floweringunder short-day conditions. AP22.65, a novel flowering-timegene in that species, was isolated and identified via genomewalkingand bioinformatics analysis. The flowering time ofAP22.65-complementing plants was similar to that of theCol-0 wild type (WT). Conversely, its overexpression delayedflowering. Consistent with this phenotype, expression ofAP22.65 was decreased in the ap22.65-1 mutant, recoveredin AP22.65-complementing plants, and increased in AP22.65-overexpressing plants. Compared with the WT, expressionlevels of critical genes in different flowering pathways, i.e.,SPY, FLC, GI, CO, FT, and LFY, were down-regulated inloss-of-function mutants. Expression of AP22.65 was distributedin flowers, siliques, rosette leaves, and whole seedlings. Therefore, this gene may be a negative regulator of Arabidopsisflowering.
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Yu-Xiang Yang,Zhen-Hua Xu,Yu-Qian Zhang,Jing Tian,Li-Xing Weng,Lian-Hui Wang 한국미생물학회 2012 The journal of microbiology Vol.50 No.6
Quorum sensing (QS) has been a novel target for the treatment of infectious diseases. Here structural analogs of Pseudomonas aeruginosa autoinducer N-acyl homoserine lactone (AHL) were investigated for QS inhibitor (QSI) activity and a novel QSI was discovered, N-decanoyl-L-homoserine benzyl ester (C2). Virulence assays showed that C2 downregulated total protease and elastase activities, as well as the production of rhamnolipid, that are controlled by QS in P.aeruginosa wild-type strain PAO1 without affecting growth. C2 was also shown to inhibit swarming motility of PAO1. Using a microdilution checkerboard method, we identified synergistic interactions between C2 and several antibiotics, tobramycin, gentamycin, cefepime, and meropenem. Data from real-time RT-PCR suggested that C2 inhibited the expression of lasR (29.67%), lasI (21.57%), rhlR (28.20%), and rhlI (29.03%).
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