Aluminum Stress Adaptation in Plants by Sanjib Kumar Panda, František Baluška

By Sanjib Kumar Panda, František Baluška

This publication is an outline of our present figuring out of aluminium toxicity and tolerance in crops. It covers all proper points from molecular and mobile biology, to genetic techniques, root biology and plant body structure. The contribution of arbuscular mycorrhizal fungi to assuaging aluminium toxicity is usually mentioned. Over forty% of overall agricultural land assets are acidic in nature, with aluminium being the foremost toxicant. Plant roots are relatively prone to aluminium tension, yet a lot of the complicated mechanism underlying its toxicity and tolerance is unknown and aluminium tension notion in vegetation continues to be poorly understood. the varied features of aluminium tension variation lined during this booklet are appropriate to plant biology scholars in any respect degrees, besides researchers and it offers a worthy contribution to our realizing of plant edition to the altering environment.

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1 and 2). For example, homologs of ALMT1 have been identified in Arabidopsis (Hoekenga et al. 2006), oilseed rape (Ligaba et al. 2006), rye (Collins et al. 2008), soybean (Liang et al. 2013), yorkshire fog (Chen et al. 2013) in addition to wheat. Genes responsible for Al-induced secretion of citrate, AACT1/MATE/FRDL (Aluminumactivated citrate transporter 1/Multidrug and toxic compound extrusion/Ferric K. F. K. Panda, F. 1007/978-3-319-19968-9_2 37 38 K. F. Ma TranscripƟonal regulaƟon mechanism Role of aluminum tolerance genes complex ?

2012). Recently, genes involved in xyloglucan metabolism in the cell wall are also reported to be involved in Al tolerance in Arabidopsis (Fig. 1; Zhu et al. 2012, 2014). For example, knockout of XTH31 resulted in an increased Al tolerance (Zhu et al. 2012). XTH31 probably encodes xyloglucan endotransglucosylase/hydrolases (XTHs), which cleaves and rejoins hemicellulosic xyloglucan polymers during cell expansion. It seems that reduction of production of cleaved xyloglucans in the cell wall increases Al tolerance.

STOP1 and STOP2 shared 40 % identity at amino acids level (Kobayashi et al. 2014). The expression level of STOP2 is much lower than that of STOP1, but the expression of STOP2 is regulated by STOP1 (Fig. 1; Sawaki et al. 2009; Kobayashi et al. 2014). Over-expression of STOP2 in stop1 mutant resulted in enhanced tolerance to low pH (Kobayashi et al. 2014). Introduction of STOP2 in stop1 mutant under the control of STOP1 promoter also complemented the expression level of ALS3 and AtMATE (Kobayashi et al.

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