JIA-2018-09

1951 XU Li-ming et al. Journal of Integrative Agriculture 2018, 17(9): 1946–1958 between the up- and down-regulated genes indicated that different regulation patterns of certain biological processes might be necessary to allow cells to redirect resources towards adaptation mechanisms or coping with Al toxicity. As “stress and defense response” and “vesicular transport” occurred in the functional classes of the up-regulated genes only, the adaptive reprogramming transcriptome for response to Al stress might require the larger number of up-regulated genes other than down-regulated genes. 3.3. Cell wall related genes response to Al stress Some studies have suggested the cell wall is the first contact site of external stimuli and Al can bind rapidly to the cell wall, then increase cell wall rigidity and reduced cell extension and growth (Sasak et al . 1996; Kochian et al . 2003; Kochian et al . 2005; Horst et al . 2010; You et al . 2011). In this study, several genes associated with the cell wall structure and modification were identified with differential expression under Al stress (Fig. 4-A). And the transcription level of pectin methylesterase ( PME ) gene (Table 1) was up-regulated by Al stress after 6 h, suggesting PME was activated by Al stress. PME activity correlated with Al adsorption capacity and Al sensitivity due to demethylation of pectin determining the amount of Al binding to the cell wall (Wen et al . 1999; Vercauteren et al . 2002). Thus, the higher level of PME activity was, the more Al-sensitive the cultivar was (Schmohl et al . 2000; Lyza et al . 2008; Yang et al . 2008). Cell wall architecture can be remodeled for alleviating Al stress (Chandran et al . 2008). And glycosyl transferases (GTs) is necessary for cell wall synthesis (Sasaki et al . 1996; Kumari et al . 2008). Typically, the sugar moieties in cell wall are predominantly glucose, galactose, fucose, glucuronic acid, and xylose (Lorenc-Kukuła et al . 2004). In the present study, five genes encoding different cell wall sugar unit transferases were increased after 6 h profile, and two genes encoding putative glucosyltransferase and GT1 were decreased at the same time point (Fig. 4-A). Recently, several reports showed that the increased expression of GT genes might enhance cell wall synthesis metabolism activity, leading to Al toxicity response in soybean (You et al . 2011) and Arabidopsis (Kumari et al . 2008). The similar results in our array indicated that the increased GTs activity with enhanced synthesis of cell wall components may cause cell wall stiffening and root cell expansion inhibition in maize, potentially representing Al toxicity response. Glycosyl transferase family 64 (GT64) (Table 1) might catalyze the formation of a glycosidic bond, that was consistent with a possible role in pectin biosynthesis, which was found in this study, Pedersen et al . (2003), and Singh et al . (2005). Sasaki et al . (1996) found that Al-sensitive plant would accumulate more lignin in the roots than Al-tolerant plant under Al stress (Sasaki et al . 1996). The shikimate and phenylpropanoid pathway were required for the biosynthesis of lignin, and phenylalanine was the final production in the shikimate pathway (Boerjan et al . 2003; Knaggs andAndrew 2003). Herrmann andWeaver (1999) and Dixon et al . (2002) reported that the genes-encoding chalcone synthase and isoflavonoid reductase related to phenylpropanoid pathway were up-regulated in soybean, leading to lignin deposition and Al-induced inhibition of root growth (Dixon et al . 2002). Similarly, one putative chalcone isomerase gene and three genes involved in the shikimate pathway, encoding shikimate kinase, shikimate dehydrogenase, and chorismate synthase, respectively, were up-regulated by Al stress after 6 h in the microarray of this study (Table 1). All these results suggested the up-regulated genes which involved in the phenylpropanoid and shikimate pathways might increase the lignin production, then lead to cell wall rigidification to resistant to Al toxicity. 3.4. Oxidative stress response genes Al stress would elicit the excessive production of reactive oxygen species (ROS), which resulting in membrane damage, chromosomal aberration, and finally cell death (Mittler et al . 2002; Yamamoto et al . 2002). Thus, many genes for detoxification of ROS components have evolved and up-regulated under Al stress, which include glutathione S -transferases (GSTs), glutaredoxins (GRXs), thioredoxins (TRXs), and lipoxygenase (LOX) genes (Kumari et al . 2008). Particularly, the transcripts abundance of GST generally represented an important protective functions against oxidative damage (Yang et al . 2001). Consistent with these results, three kinds of antioxidant enzymes, GST, GRXs, and TRX, were also identified in this study, and the increased transcripts for GST , tetratricopetide-repeat TRX , and TRX genes were also detected after 6 h of Al exposure (Table 1). Additionally, a unique GRX4 gene with 52% similarity to AtGRX4 sequence was up-regulated by Al stress after 6 h in this study. Tetratricopetide-repeat TRX and TRX are both involved in plant oxidoreduction activities (Sang et al . 2010; Meyer et al . 2012). And GRXs are members of the TRX fold protein family (Cheng et al . 2006). The AtGRX 4 gene in Arabidopsis was induced by various environment stimuli such as temperature and metal-ion stress, and the seedlings root of atgrx4 mutants were more sensitive to oxidants than wild seedlings (Cheng et al . 2008). Basing on the results, GS T, tetratricopetide-repeat TRX , TRX , and GRX4 genes may scavenge ROS activity, thus resulting in a strong maize Al tolerance.