Xanthomonas oryzae pv. oryzae avirulence genes contribute differently and specifically to pathogen aggressiveness
Xanthomonas oryzae pv. oryzae avirulence genes contribute differently and specifically to pathogen aggressiveness
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DOI：
10.1094/mpmi.2000.13.12.1322
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发表时间：
2000-12-01
影响因子：
3.5
通讯作者：
Leach, JE
中科院分区：
文献类型：
--
作者：
Bai, JF;Choi, SH;Leach, JE
对3株水稻白叶枯病菌（Xanthomonas oryzae pv.以水稻无毒基因avrXa7、avrXa10和avrXa5和4个同源基因aB3.5、aB3.6、aB4.3和aB4.5为材料，分别或联合诱变，攻击性或疾病X的数量。oryzaepv.稻瘟病菌在感病水稻品系中的致病性。这些X。oryzaepv.水稻基因是高度相关的黄单胞菌avrBs3基因家族的成员。与野生型菌株相比，X. oryzaepv.在avrXa7、avrxa5和4个同源基因中具有突变的水稻菌株在水稻品系IR24上引起较短的损害，该品系不含有与野生型菌株相关的抗性基因。每个基因对病变长度的贡献各不相同，avrXa7贡献最大，avrXa10对侵袭性没有可测量的影响。avrXa7、aB4.5和avrxa5的功能性质粒携带拷贝仅分别恢复了对avrXa7、aB4.5和avrxa5突变株的攻击性。avrXa7中的突变不能由携带任何其他avr基因家族成员的质粒互补。这些数据表明，avr家族的一些成员，但不是全部，对病原体的侵袭性有贡献，而且这些贡献在数量上是不同的。此外，尽管它们的序列相似，但这些基因家族成员的攻击性功能是不可互换的。这些结果表明，选择和聚合抗性基因可以通过适应度惩罚的程度来指导，这是经验确定的avr基因突变。
Genomic copies of three Xanthomonas oryzae pv. oryzae avirulence (avr) genes, avrXa7, avrXa10, and avrxa5, and four homologous genes, aB3.5, aB3.6, aB4.3, and aB4.5, were mutagenized individually or in combination to study the roles of avr genes in one component of pathogen fitness, i.e., aggressiveness or the amount of disease X. oryzae pv. oryzae causes in susceptible rice lines. These X. oryzae pv. oryzae genes are members of the highly related Xanthomonas avrBs3 gene family. Compared to the wild-type strain, X. oryzae pv. oryzae strains with mutations in avrXa7, avrxa5, and the four homologous genes caused shorter lesions on rice line IR24, which contains no resistance genes relevant to the wild-type strain. The contribution of each gene to lesion length varied, with avrXa7 contributing the most and avrXa10 showing no measurable effect on aggressiveness. The functional, plasmidborne copies of avrXa7, aB4.5, and avrxa5 restored aggressiveness only to strains with mutations in avrXa7, aB4.5, and avrxa5, respectively. Mutations in avrXa7 were not complemented by plasmids carrying any other avr gene family members. These data indicate that some, but not all, avr family members contribute to pathogen aggressiveness and that the contributions are quantitatively different. Furthermore, despite their sequence similarity, the aggressiveness functions of these gene family members are not interchangeable. The results suggest that selection and pyramiding resistance genes can be guided by the degree of fitness penalty that is empirically determined in avr gene mutations.