Shim Isaac, Law Robert, Kileeg Zachary, Stronghill Patricia, Northey Julian G B, Strap Janice L, Bonetta Dario T
Faculty of Science, University of Ontario Institute of Technology, Oshawa, ON, Canada.
Department of Biological Sciences, University of Toronto Scarborough Campus, Toronto, ON, Canada.
Front Plant Sci. 2018 Aug 24;9:1152. doi: 10.3389/fpls.2018.01152. eCollection 2018.
The cellulose synthase (CESA) proteins in play an essential role in the production of cellulose in the cell walls. Herbicides such as isoxaben and flupoxam specifically target this production process and are prominent cellulose biosynthesis inhibitors (CBIs). Forward genetic screens in revealed that mutations that can result in varying degrees of resistance to either isoxaben or flupoxam CBI can be attributed to single amino acid substitutions in primary wall CESAs. Missense mutations were almost exclusively present in the predicted transmembrane regions of CESA1, CESA3, and CESA6. Resistance to isoxaben was also conferred by modification to the catalytic residues of CESA3. This resulted in cellulose deficient phenotypes characterized by reduced crystallinity and dwarfism. However, mapping of mutations to the transmembrane regions also lead to growth phenotypes and altered cellulose crystallinity phenotypes. These results provide further genetic evidence supporting the involvement of CESA transmembrane regions in cellulose biosynthesis.
植物中的纤维素合酶(CESA)蛋白在细胞壁纤维素的合成过程中发挥着至关重要的作用。异恶草酮和氟草胺等除草剂专门针对这一生产过程,是典型的纤维素生物合成抑制剂(CBI)。在植物中进行的正向遗传学筛选表明,能够导致对异恶草酮或氟草胺CBI产生不同程度抗性的突变可归因于初生壁CESA中的单个氨基酸替换。错义突变几乎只存在于CESA1、CESA3和CESA6的预测跨膜区域。对CESA3催化残基的修饰也赋予了对异恶草酮的抗性。这导致了纤维素缺乏的表型,其特征是结晶度降低和植株矮小。然而,将突变定位到跨膜区域也导致了生长表型和纤维素结晶度改变的表型。这些结果提供了进一步的遗传学证据,支持CESA跨膜区域参与纤维素生物合成。