Because plants are sessile organisms and they cannot move when they are exposed to a stress such as cadmium, they have developed different mechanisms to survive to the metal: (1) accumulate it; (2) prevent its entry or (3) exclude it once it is in the plant tissue (Watanabe et al. 2010):
1. A group of plants, called hyperaccumulators, tolerate Cd accumulation without toxicity symptoms (Verbruggen et al. 2009). Cd hyperaccumulation is present only in some populations of Sedum alfredii, Thlaspi caerulescens, Thlaspi praecox and Arabidopsis halleri which are able to hyperaccumulate Cd which is taken up in part through Zn transporters (Zhao et al. 2006). It has been described that peroxidases played an important role during Cd hyperaccumulation, and the accumulation of ROS induced by Cd treatment might be involved in the metal hyperaccumulation (Zhang and Qiu 2007). In Arabidopsis thaliana a cadmium-tolerant mutant (MRC-32) has been identified that accumulates more Cd than wild-type (WT) plants although the mechanism involved in this hyperaccumulation has not yet been identified (Watanabe et al. 2010).
2. At root level, plants have developed extracellular strategies to avoid Cd toxicity and especially interesting is the relationship with mycorrhizal fungus (Jentschke et al. 1999; Courbot et al. 2004; Janouskova et al. 2006) or with some bacterial strains from the rhizosphere which can reduce Cd concentration in the shoot of the hyperaccumulators A. halleri, and which highlights the importance of plant-microbe interactions in Cd toxicity (Farinati et al. 2011). Additionally, the evaluation of interactions between heavy metal contamination and beneficial rhizosphere microbes adapted to the contaminated soils and their effects on plant development has shown that the microbes are not only able to grow but also to improve plant development under polluted conditions (Azcon et al. 2010). Interestingly, it seems that toxicity of heavy metal to microorganisms is due, in part, to oxidative stress, and it has been hypothesised that the metal resistance of microorganisms and their beneficial effect on the plant can be ascribed partially to the microbe antioxidative enzyme metabolism (Azcon et al. 2010). Moreover, there are other mechanisms like the immobilisation of Cd by means of the cellular and extracellular carbohydrates (Verkleij and Schat 1990; Wagner 1993). Recently, a Cd-phobic mutant (MRC-22) has been shown to arrest the growth of the primary root immediately when it encounters Cd and to produce an increased number of lateral roots located in the Cd-free zone (Watanabe et al. 2010). Some authors have suggested that the primary root could act as a sensor of the root environment and send some cues to the whole root system to modulate the direction of root growth, MRC-22 could be affected in this sensitivity sending more cues than WT on encountering Cd (Watanabe et al. 2010).
3. Plants have also developed intracellular strategies against Cd toxicity such as transport to the major storage organs or tissues, chelation and subcellular com-partmentalization and the efflux from the plant (Benavides et al. 2005; Verbruggen et al. 2009; Sharma and Dietz 2009). As described previously, Cd enters first by the roots through the cortical tissue. Roots accumulate Cd during its exposure and part of the metal is then translocated to leaves (Ogawa et al. 2009). Cd can be loaded rapidly into the xylem by transport to the above-ground tissues. Once Cd has entered into the cytosol, it can bind to phytochelatins or their precursor glutathione, generating conjugates that can be transported into the vacuoles, preventing the free circulation of Cd ions in the cytosol (Cobbett 2000; Verbruggen et al. 2009). Cd can also be complexated by metallothioneins and nicotianamine (Cobbett and Goldsbrough 2002; Sharma and Dietz 2006). Proline, histidine and polyamines are also involved in the defence against metal stress because they may be involved in osmoregulation and metal chelation, or they can act as antioxidants (Sharma and Dietz 2006). Referring to compartmen-talisation of Cd, it has been shown that some of the genes regulated by Cd are involved in its own transport, like AtPcrl (Song et al. 2004). It seems that soluble phenols may be involved in Cd shoot-to-root translocation as a result of SA treatment (Kovacik et al. 2009). Translocation of Cd from root to shoots is mainly done through inorganic forms (Ueno et al. 2008), although Cd2+ can be directly transported into the vacuoles by Cd2+/proton antiporter (Korenkov et al. 2007; Berezin et al. 2008) and the metal transporters NRAMP3 and NRAMP4 are responsible for Cd2+ efflux from vacuoles (Thomine et al. 2000, 2003). For the translocation of Cd, plants partially share the processes with Zn and/or Fe transport, like the Zn transporter ZNT1 that can also transport Cd, but with a lower affinity than with Zn (Pence et al. 2000; Ueno et al. 2008). The MRC-26 gene could be involved in the Cd transport from root to aerial tissues (Watanabe et al. 2010) and originally it was a defective mutant in Fe absorption or Fe transport from roots to the aboveground tissues. Very recently, a novel molecular mechanism of heavy metal tolerance in plants has been ascribed to microRNAs (miRNAs) that are small non-coding RNAs that negatively regulate specific target mRNAs at the post-transcriptional level. In fact, a total of 19 Cd-responsive miRNAs have been identified in rice which encoded transcription factors (TFs) and proteins associated with metabolic processes or stress responses (Ding et al. 2011). Many of the predicted target genes of the Cd-responsive miRNAs encode TFs and as most of the miRNAs are down-regulated, the target of these TFs will be up-regulated leading to enhanced Cd tolerance (Ding et al. 2011). Plants have also developed other strategies to cope with Cd like activation of genes involved in defence responses, production of ROS and NO and modifications of antioxidant systems that will be discussed in the following paragraphs.
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