analysis of vascular development in the hydra sterol biosynthetic mutants of arabidopsis分析血管发展的九头蛇甾醇生物合成的拟南芥的突变体.pdfVIP

analysis of vascular development in the hydra sterol biosynthetic mutants of arabidopsis分析血管发展的九头蛇甾醇生物合成的拟南芥的突变体.pdf

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analysis of vascular development in the hydra sterol biosynthetic mutants of arabidopsis分析血管发展的九头蛇甾醇生物合成的拟南芥的突变体

Analysis of Vascular Development in the hydra Sterol Biosynthetic Mutants of Arabidopsis ¤ Margaret Pullen, Nick Clark, Fatemeh Zarinkamar , Jennifer Topping, Keith Lindsey* The Integrative Cell Biology Laboratory, School of Biological and Biomedical Sciences, Durham University, Durham, United Kingdom Abstract Background: The control of vascular tissue development in plants is influenced by diverse hormonal signals, but their interactions during this process are not well understood. Wild-type sterol profiles are essential for growth, tissue patterning and signalling processes in plant development, and are required for regulated vascular patterning. Methodology/Principal Findings: Here we investigate the roles of sterols in vascular tissue development, through an analysis of the Arabidopsis mutants hydra1 and fackel/hydra2, which are defective in the enzymes sterol isomerase and sterol C-14 reductase respectively. We show that defective vascular patterning in the shoot is associated with ectopic cell divisions. Expression of the auxin-regulated AtHB8 homeobox gene is disrupted in mutant embryos and seedlings, associated with variably incomplete vascular strand formation and duplication of the longitudinal axis. Misexpression of the auxin reporter proIAA2:GUS and mislocalization of PIN proteins occurs in the mutants. Introduction of the ethylene-insensitive ein2 mutation partially rescues defective cell division, localization of PIN proteins, and vascular strand development. Conclusions: The results support a model in which sterols are required for correct auxin and ethylene crosstalk to regulate PIN localization, auxin distribution and AtHB8 expression, necessary for correct vascular development. Citation: Pullen M, Clar

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