Vélez-Bermúdez Isabel-Cristina, Salazar-Henao Jorge E, Fornalé Silvia, López-Vidriero Irene, Franco-Zorrilla José-Manuel, Grotewold Erich, Gray John, Solano Roberto, Schmidt Wolfgang, Pagés Montserrat, Riera Marta, Caparros-Ruiz David
Centre de Recerca en Agrigenòmica, Consortium CSIC-IRTA-UAB-UB, Cerdanyola del Vallès, 08193 Barcelona, Spain Institute of Plant and Microbial Biology, Academia Sinica, 11529 Taipei, Taiwan.
Centre de Recerca en Agrigenòmica, Consortium CSIC-IRTA-UAB-UB, Cerdanyola del Vallès, 08193 Barcelona, Spain.
Plant Cell. 2015 Nov;27(11):3245-59. doi: 10.1105/tpc.15.00545. Epub 2015 Nov 13.
Lignin is an essential polymer in vascular plants that plays key structural roles in vessels and fibers. Lignification is induced by external inputs such as wounding, but the molecular mechanisms that link this stress to lignification remain largely unknown. In this work, we provide evidence that three maize (Zea mays) lignin repressors, MYB11, MYB31, and MYB42, participate in wound-induced lignification by interacting with ZML2, a protein belonging to the TIFY family. We determined that the three R2R3-MYB factors and ZML2 bind in vivo to AC-rich and GAT(A/C) cis-elements, respectively, present in a set of lignin genes. In particular, we show that MYB11 and ZML2 bind simultaneously to the AC-rich and GAT(A/C) cis-elements present in the promoter of the caffeic acid O-methyl transferase (comt) gene. We show that, like the R2R3-MYB factors, ZML2 also acts as a transcriptional repressor. We found that upon wounding and methyl jasmonate treatments, MYB11 and ZML2 proteins are degraded and comt transcription is induced. Based on these results, we propose a molecular regulatory mechanism involving a MYB/ZML complex in which wound-induced lignification can be achieved by the derepression of a set of lignin genes.
木质素是维管植物中的一种重要聚合物,在导管和纤维中发挥关键的结构作用。木质化是由诸如创伤等外部刺激诱导的,但将这种胁迫与木质化联系起来的分子机制在很大程度上仍不清楚。在这项研究中,我们提供证据表明,三种玉米(Zea mays)木质素抑制因子MYB11、MYB31和MYB42,通过与属于TIFY家族的蛋白质ZML2相互作用,参与创伤诱导的木质化过程。我们确定这三种R2R3-MYB因子和ZML2在体内分别与一组木质素基因中存在的富含AC和GAT(A/C)的顺式元件结合。特别是,我们表明MYB11和ZML2同时结合到咖啡酸O-甲基转移酶(comt)基因启动子中存在的富含AC和GAT(A/C)的顺式元件上。我们表明,与R2R3-MYB因子一样,ZML2也作为转录抑制因子发挥作用。我们发现,在创伤和茉莉酸甲酯处理后,MYB11和ZML2蛋白被降解,comt转录被诱导。基于这些结果,我们提出了一种涉及MYB/ZML复合物的分子调控机制,其中创伤诱导的木质化可以通过一组木质素基因的去抑制来实现。