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The Class II KNOX genes KNAT3 and KNAT7 work cooperatively to influence deposition of secondary cell walls that provide mechanical support to Arabidopsis stems
First author: Shumin Wang; Affiliations: University of British Columbia (不列顛哥倫比亞大學): Vancouver, Canada
Corresponding author: Shawn D. Mansfield
The transcription factor KNOTTED ARABIDOPSIS THALIANA7 (KNAT7) is a Class II KNOTTED1‐like homeobox (KNOX2) gene that, in interfascicular fibres, acts as a negative regulator of secondary cell wall biosynthesis. In addition, knat7 loss‐of‐function mutants display an irregular xylem (irx) phenotype, suggesting a potential positive regulatory role in xylem vessel secondary cell wall deposition. Although our understanding of the role of KNAT7 is evolving, the function(s) of the closely related KNOX2 genes, KNAT3, KNAT4, and KNAT5, in secondary wall formation still remain unclear. We found that all four Arabidopsis KNOX2 genes were expressed in the inflorescence stems. However, only the knat3 knat7 double mutants showed a phenotype, displaying an enhanced irx phenotypes relative to the single mutants, as well as decreased interfascicular fibre cell wall thickness. Moreover, knat3 knat7 double mutants had reduced stem tensile and flexural strength compared with wild‐type and single mutants. In contrast, KNAT3 overexpression resulted in thicker interfascicular fibre secondary cell walls in inflorescence stems, suggesting a potential positive regulation in interfascicular fibre secondary wall development. This work identifies KNAT3 as a potential transcriptional activator working together with KNAT7 to promote secondary cell wall biosynthesis in xylem vessels, while concurrently acting antagonistically with KNAT7 to influence secondary wall formation in interfascicular fibres.
轉錄因子KNAT7是一個II類KNOTTED1同源異型基因KNOX2，其在束間纖維中充當次生細胞壁生物合成的負調節因子發揮作用。另外，knat7功能缺失突變體顯示出不規則的木質部表型，說明其可能在木質部導管次生細胞壁沉積方面發揮正向調控作用。儘管我們對於KNA7基因功能的了解逐日增加，但是其近緣基因KNAT3/4/5在次生細胞壁形成方面的作用仍不清楚。本文的，作者發現四個擬南芥KNOX2基因都在花序莖中表達。然而，僅有knat3 knat7雙突變體存在明顯的表型，相比於單突變體而言，不規則木質部表型缺陷更加強烈，而且束間纖維細胞壁厚度降低。此外，相比於野生型和單突變體，knat3 knat7雙突變體莖的抗拉和抗彎強度均有所下降。相反，KNAT3過表達會導致花序莖中較厚的束間纖維次生細胞壁，說明其在束間纖維次生細胞壁發育過程中存在正向的調控作用。本文的工作鑑定了KNAT3基因作為一個潛在的轉錄激活因子，與KNAT7基因一起作用於木質部導管中的次生細胞壁生物合成，但在束間纖維中與KNAT7拮抗，影響次生細胞壁的形成。
通訊：Shawn D. Mansfield (http://profiles.forestry.ubc.ca/person/shawn-mansfield/)
研究方向：林木生物技術；基因表達和細胞壁發育性狀的表型之間的關係；植物代謝組；細胞壁發育；纖維素生物合成；木質素生物合成；蔗糖代謝；人為汙染（磷，鹽，重金屬）的修復。
doi: https://doi.org/10.1111/tpj.14541
Journal: the plant journal
First Published: October 06, 2019