Zhu W, Yang B, Chittoor J M, Johnson L B, White F F
Department of Plant Pathology, Kansas State University, Manhattan 66506, USA.
Mol Plant Microbe Interact. 1998 Aug;11(8):824-32. doi: 10.1094/MPMI.1998.11.8.824.
The avrXa10 gene of Xanthomonas oryzae pv. oryzae, the causal agent of bacterial blight of rice, is a member of the avrBs3 avirulence gene family and directs the elicitation of resistance in a gene-for-gene manner on rice lines carrying the resistance gene Xa10. The carboxyl (C) terminus of AvrXa10 has a previously undescribed domain that is structurally similar to the acidic activation domain of many eukaryotic transcription factors in addition to three nuclear localization signal (NLS) sequences. Removal of the C-terminal 38 codons containing the putative activation domain, but retaining the NLS sequences, was concomitant with the loss of avirulence activity. The C-terminal coding regions of avrBs3 and avrXa7 can be replaced by the corresponding region of avrXa10, and the genes retained specificity for the resistance genes Bs3 in pepper and Xa7 in rice, respectively. The avrBs3 and avrXa7 avirulence activities of the hybrid genes were also lost upon removal of the terminal 38 codons. When fused to the coding sequence of the Gal4 DNA binding domain, AvrXa10 activated transcription in yeast and Arabidopsis thaliana. Removal of the carboxyl region severely reduced transcriptional activation. AvrXa10 would have to be localized to the host cell nucleus to function autonomously in transcriptional activation. Consistent with this requirement, mutations in all three NLS sequences of avrXa10 caused a loss in avirulence activity. The findings demonstrate the requirement of the C terminus for AvrXa10 function and the potential for the members of this family of avirulence gene products to enter the host nucleus and alter host transcription.
水稻白叶枯病的病原菌——水稻白叶枯菌（Xanthomonas oryzae pv. oryzae）的avrXa10基因是avrBs3无毒基因家族的成员之一，它能以基因对基因的方式，在携带抗病基因Xa10的水稻品系中引发抗性。AvrXa10的羧基（C）末端有一个之前未被描述的结构域，该结构域除了含有三个核定位信号（NLS）序列外，其结构与许多真核转录因子的酸性激活结构域相似。去除包含假定激活结构域的C末端38个密码子，但保留NLS序列，会导致无毒活性丧失。avrBs3和avrXa7的C末端编码区可以被avrXa10的相应区域取代，并且这些基因分别对辣椒中的抗病基因Bs3和水稻中的Xa7保持特异性。去除末端38个密码子后，杂合基因的avrBs3和avrXa7无毒活性也会丧失。当与Gal4 DNA结合结构域的编码序列融合时，AvrXa10能在酵母和拟南芥中激活转录。去除羧基区域会严重降低转录激活。AvrXa10必须定位于宿主细胞核才能在转录激活中自主发挥作用。与此要求一致的是，avrXa10所有三个NLS序列中的突变都会导致无毒活性丧失。这些发现证明了C末端对AvrXa10功能的必要性，以及该无毒基因家族成员进入宿主细胞核并改变宿主转录的可能性。
