SHEPHERD is the Arabidopsis GRP94 responsible for the formation of functional CLAVATA proteins
SHEPHERD is the Arabidopsis GRP94 responsible for the formation of functional CLAVATA proteins
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DOI：
10.1093/emboj/21.5.898
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发表时间：
2002-03-01
期刊：
影响因子：
11.4
通讯作者：
Okada, K
中科院分区：
文献类型：
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作者：
Ishiguro, S;Watanabe, Y;Okada, K
拟南芥牧羊人（shd）突变体表现出扩大的茎顶端分生组织（SAM）和花分生组织（FM），混乱的根顶端分生组织，和花粉管伸长的缺陷。我们已经发现SHD编码GRP 94的直系同源物，GRP 94是ER驻留的HSP 90样蛋白。由于SAM和FM中的SHD表型与clv突变体相似，我们探索了CLV复合体成员可能是SHD靶点的可能性。shd clv双突变体的SAM和FM形态与clv单突变体的SAM和FM形态无法区分，并且wuschel（wus）突变对shd突变是完全上位性的，表明SHD和CLV在相同的遗传途径中起作用以抑制WUS功能。此外，CLV 3过表达的影响，导致SAM活性的消除被取消的shd突变体，表明CLV功能依赖于SHD功能。因此，我们得出结论，SHD蛋白的正确折叠和/或复杂的CLV蛋白的形成是必需的。
The Arabidopsis shepherd (shd) mutant shows expanded shoot apical meristems (SAM) and floral meristems (FM), disorganized root apical meristems, and defects in pollen tube elongation. We have discovered that SHD encodes an ortholog of GRP94, an ER-resident HSP90-like protein. Since the shd phenotypes in SAM and FM are similar to those of the clavata (clv) mutants, we have explored the possibility that CLV complex members could be SHD targets. The SAM and FM morphology of shd clv double mutants are indistinguishable from those of clv single mutants, and the wuschel (wus) mutation is completely epistatic to the shd mutation, indicating that SHD and CLV act in the same genetic pathway to suppress WUS function. Moreover, the effects of CLV3 overexpression that result in the elimination of SAM activity were abolished in the shd mutant, indicating that CLV function is dependent on SHD function. Therefore, we conclude that the SHD protein is required for the correct folding and/or complex formation of CLV proteins.