Zhu Yi-Fang, Guo Jinliang, Zhang Yang, Huang Chao-Feng
College of Resources and Environmental Sciences, Nanjing Agricultural University, Nanjing, China.
Shanghai Center for Plant Stress Biology and National Key Laboratory of Plant Molecular Genetics, CAS Center for Excellence in Molecular Plant Sciences, Chinese Academy of Sciences, Shanghai, China.
Front Plant Sci. 2021 Jul 12;12:698443. doi: 10.3389/fpls.2021.698443. eCollection 2021.
The C2H2-type zinc finger transcription factor SENSITIVE TO PROTON RHIZOTOXICITY 1 (STOP1) plays a critical role in aluminum (Al) resistance and low phosphate (Pi) response mainly through promoting the expression of the malate transporter-encoding gene . We previously showed that REGULATION OF ATALMT1 EXPRESSION 3 (RAE3/HPR1), a core component of the THO/TREX complex, is involved in the regulation of nucleocytoplasmic mRNA export to modulate Al resistance and low Pi response. Here, we report that RAE2/TEX1, another core component of the THO complex, is also involved in the regulation of Al resistance and low Pi response. Mutation of reduced the expression of STOP1-downstream genes, including . was less sensitive to Al than , which was consistent with less amount of malate secreted from roots than from roots. Nevertheless, low Pi response was impaired more in than in , suggesting that RAE2 also regulates AtALMT1-independent pathway to modulate low Pi response. Furthermore, unlike RAE3 that regulates mRNA export, mutating did not affect mRNA accumulation in the nucleus, although STOP1 protein level was reduced in . Introduction of mutation into mutant background could partially recover the deficient phenotypes of . Together, our results demonstrate that RAE2 and RAE3 play overlapping but distinct roles in the modulation of Al resistance and low Pi response.
C2H2型锌指转录因子质子根毒性敏感1（STOP1）在耐铝（Al）和低磷（Pi）响应中起关键作用，主要通过促进苹果酸转运蛋白编码基因的表达来实现。我们之前表明，THO/TREX复合物的核心成分——ATALMT1表达调控3（RAE3/HPR1）参与调节核质mRNA输出，以调节耐铝性和低磷响应。在此，我们报道THO复合物的另一个核心成分RAE2/TEX1也参与耐铝性和低磷响应的调节。RAE2突变降低了包括……在内的STOP1下游基因的表达。RAE2突变体对铝的敏感性低于野生型，这与RAE2突变体根系分泌的苹果酸量少于野生型根系一致。然而，RAE2突变体的低磷响应比野生型受到的损害更大，这表明RAE2也调节不依赖AtALMT1的途径来调节低磷响应。此外，与调节mRNA输出的RAE3不同，突变RAE2不会影响mRNA在细胞核中的积累，尽管RAE2突变体中STOP1蛋白水平降低。将RAE2突变引入RAE3突变背景中可以部分恢复RAE3突变体的缺陷表型。总之，我们的结果表明RAE2和RAE3在调节耐铝性和低磷响应中发挥重叠但不同的作用。
