Resistance against herbicide isoxaben and cellulose deficiency caused by distinct mutations in same cellulose synthase isoform CESA6
Resistance against herbicide isoxaben and cellulose deficiency caused by distinct mutations in same cellulose synthase isoform CESA6
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DOI：
10.1104/pp.010822
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发表时间：
2002-02-01
期刊：
影响因子：
7.4
通讯作者：
Höfte, H
中科院分区：
文献类型：
--
作者：
Desprez, T;Vernhettes, S;Höfte, H
异恶酰草胺是一种芽前除草剂，可抑制高等植物中的纤维素生物合成。在拟南芥中发现了两个由异恶苯抗性突变体（ixr 1 -1、ixr 1 -2和ixr 2 -1）鉴定的基因座。最近显示IXR 1编码纤维素合酶催化亚基CESA 3（W.- R.沙伊布勒河埃谢德，T。里士满，D. Delmer和C.萨默维尔[2001] Proc Natl Acad Sci USA 98：10079-10084）。在这里，我们报告IXR 2的克隆，并显示它编码另一种纤维素合酶亚型，CESA 6。ixr 2 -1携带取代CESA 6的C末端附近的氨基酸的突变，该氨基酸在CESA家族成员中高度保守。用突变基因而不是野生型基因转化野生型植物赋予了对除草剂的抗性增加。对这两个异恶苯耐药基因座存在的最简单解释是CESA 3和CESA 6具有冗余功能。然而，CESA 6的功能丧失procuste 1等位基因先前被证明具有强烈的生长缺陷，并降低了根和黑暗生长的下胚轴中的纤维素含量。这表明在这些突变体中，CESA 3的存在并不能补偿根和黑暗生长的下胚轴中CESA 6的缺失，这与CESA 3和CESA 6的冗余功能相矛盾。总之，这些观察结果与CESA 6和CESA 3作为蛋白质复合物具有活性的模型兼容。
Isoxaben is a pre-emergence herbicide that inhibits cellulose biosynthesis in higher plants. Two loci identified by isoxaben-resistant mutants (ixr1-1 ixr1-2, and ixr2-1) in Arabidopsis have been reported previously. IXR1 was recently shown to encode the cellulose synthase catalytic subunit CESA3 (W.-R. Scheible, R. Eshed, T. Richmond, D. Delmer, and C. Somerville [2001] Proc Natl Acad Sci USA 98: 10079-10084). Here, we report on the cloning of IXR2, and show that it encodes another cellulose synthase isoform, CESA6. ixr2-1 carries a mutation substituting an amino acid close to the C terminus of CESA6 that is highly conserved among CESA family members. Transformation of wild-type plants with the mutated gene and not with the wild-type gene conferred increased resistance against the herbicide. The simplest interpretation for the existence of these two isoxaben-resistant loci is that CESA3 and CESA6 have redundant functions. However, loss of function procuste1 alleles of CESA6 were previously shown to have a strong growth defect and reduced cellulose content in roots and dark-grown hypocotyls. This indicates that in these mutants, the presence of CESA3 does not compensate for the absence of CESA6 in roots and dark-grown hypocotyls, which argues against redundant functions for CESA3 and CESA6. Together, these observations are compatible with a model in which CESA6 and CESA3 are active as a protein complex.