Aluminum (Al) toxicity is a principle constraint in acidic soils and widespread areas of rice planting from tropical regions (Ismail et al., 2007). Aluminum is solubilized as Al3+ into the soil solution in intense acidic soil conditions, Al3+ is highly phytotoxic, causing a quick deterrence of the root growth that ultimately, decreased and stunted root system, therefore influencing the capability of a plant to uptake both nutrients and water (Famoso et al., 2011).
In some studies, has been illustrated that levels of tolerance to Al toxicity differences between and within species. In addition, great Al tolerance in both hydroponic and field conditions have been demonstrated in rice genotypes (Foy, 1988; Kochian et al., 2005; Famoso et al., 2010;). However, rice is approximately 6 to 10 times more aluminum tolerant than other cereals, less is studied on the genes involving this tolerance. Considering to great level of Al tolerance and good genetic resources, rice furnished a well model for assessing the physiology and genetics of Al tolerance (Famoso et al., 2011). A potential mechanism dealing with Al accumulation tolerance in shoot and root tissue via internal detoxification (Ma, et al., 1998).
There is good variation between varieties in terms of Al tolerance, several QTLs identified using a population derived from sensitive IR64 and tolerant Azucena cross for shoot weight, leaf bronzing, and iron concentration (Wu et al., 1997, 1998). There has been difficulty in screening using a hydroponic system, owing to quickly reducing iron content in solution culture, although a developed screening approaches that could recognizing sensitive and tolerance varieties have and used for more accurate genetic studies (Shimizu, et al., 2005).
The effort to cope with aluminum toxicity
Rice (Oryza sativa L.) is less susceptible to Al toxicity than other cereals (Ma, 2007; Famoso et al., 2010), furthermore, there is a genotypic distinction among japonica and indica cultivars. Several transcriptional factors have been identified for aluminum tolerance in rice including Al resistance transcription factor 1 (ART1), Nramp aluminum transporter 1 (Nrat1), stress and ripening 5 (ASR5), and WRKY22 (Yamaji et al., 2009; Arenhart et al., 2014; Li et al., 2018). All genes that are responsive to Al toxicity have essential tasks to carry out towards plant Al tolerance. ART1 regulates the external and internal detoxification of Al by influencing about 30 genes (Yamaji et al., 2009; Ma, et al., 2014). Nrat1, intercedes the transportation of trivalent Al into root cells (Xia et al., 2010). Diminishing Al uptake, enhancing Al binding to the cell wall, and enhancement of Al affectability, are the results of Nrat1 silencing. The genotypic distinction in Al tolerance in rice may incompletely clarify by diverse expression of Nrat1 (Li et al., 2014; Xia et al., 2014).
Aluminum tolerance is a complex trait governed by various genes/QTLs in rice. OsALS1 is a single-copy gene in the rice genome that have a main role in Al tolerance in rice. It encodes a transporter that possibly intervene subsequent detoxification through transport and Al aggregation into cell vacuoles (Xia et al., 2010; Simoes et al., 2012; Huang et al., 2012). In general, of 148 QTLs were reported for Al tolerance in rice using linkage mapping by biparental crosses (Wu et al., 2000; Nguyen et al., 2001; Ma et al., 2002; Nguyen et al., 2002; Nguyen et al., 2003; Mao et al., 2004; Xue et al., 2006; Xue et al., 2007; Ma et al., 2009) and association mapping using natural populations (Famoso et al., 2011; Zhang et al., 2016). Al tolerant QTL including a large effect ART1 located on chromosome 12 with LOD = 7.85 and R2 = 19.3% using a RIL population. In addition, three genomic regions encompassing STAR2, ART1, and Nrat1 related to induced Al-sensitive of rice mutants were detected using biparental mapping population (Famoso et al., 2011). Genome wide association study for relative root elongation was conducted by a diverse panel consisting of 150 rice landraces, the PSM365 explained meaningful associations (20.03%) located at 21.4 Mb on chromosome 11 (Zhang et al., 2016).
Recently, the multi-parent advanced generation inter-cross (MAGIC) populations were mapped using a 55 K rice SNP array and phenotype at the seedling stage for Zn, Fe, and Al under a hydroponics system. A total of 30, 21, and 21 QTL were detected for Zn, Fe, and Al toxicity tolerance, respectively. For multi tolerance of Fe, Zn, and Al affiliated traits, three genomic regions, MT3.2 on chromosome 3 (35.4-36.2Mb), MT1.2 on chromosome 1 (35.4–36.3Mb), and MT1.1 on chromosome 1 (35.4–36.3Mb) QTLs have been identified. The chromosomal regions MT2.3 on chromosome 2 (30.5–31.6Mb), MT3.1 on chromosome 3 (12.5–12.8Mb), and MT6 on chromosome 6 (2.0–3.0Mb) possessed QTLs for Zn and Al tolerance. The QTL (MT9.1) for Fe and Al tolerance located on chromosomal 9 (14.2–14.7Mb) (Meng et al., 2017).
Iron (Fe) is a fundamental microelement which is managing distinctive essential mechanisms in plants. Through the redox status modify among the ferrous (Fe2+) and ferric (Fe3+) shape, Fe task as an electron acceptor or donor, that is essential in the mechanisms in photosynthesis and respiration (Kobayashi and Nishizawa, 2012; Zhai et al., 2014). In addition, Fe plays as a co-factor of numerous enzymes (Briat and Lobreaux, 1997; Wu, et al., 2017).
although its necessary as a plant nutrient, the excess amount of Fe can form toxicity in plant (Wu et al., 2014). Iron toxicity is appeared once a vast amount of Fe (II) is accumulating in situ in soil solution, also, once interflow fetches ions of Fe (II) from upper slopes (Ponnamperuma, 1972; Yoshida, 1981). The iron toxicity in rice plant appears once the toxic concentration of Fe accumulates in leaves. The incidence of Fe toxicity is related to the excess concentration of Fe(II) in the soil solution (Ponnamperuma, et al., 1955).
Iron deficiency causes chlorosis among the leaves veins and the deficiency symptom appears initially in the plant’s young leaves (Das, 2014). Iron toxicity leads to oxidative stress through the Fenton reaction (Wu et al., 2017), due to toxicity of Fe, rice yield usually losses from 12-100% (Sahrawat, 2004). Leaf bronzing in rice is one of the visible Fe toxicity symptoms, which arise with decreasing of root and shoot growth (Wu et al., 2014). Discoloration of leaf and the leaf bronzing index (LBI) are both usage for evaluating the vastness of Zn toxicity (Frei, et al., 2010; Höller, et al., 2014; Wu et al., 2014; Meng et al., 2017).
Tolerance mechanisms and interaction of iron with other nutrients
An excess iron concentration in the soil solution may cause nutrient imbalance via antagonistic impact on the acquisition of nutrients, including K, P, Mn and Zn (Ramírez, et al., 2002; Fageria, et al., 2008; Sahrawat, 2004, 2008, 2010). Various mechanisms were recognized for tolerance to Fe toxicity such as Root based tolerance and shoot based tolerance. Root based mechanisms based on using a physical barrier that preventing excess iron absorption (Becker ; Asch, 2005; Wu et al., 2014, 2017). Shoot based tolerance mechanisms consist of maintaining iron in less active photosynthesis tissues such as stem (Engel, et al., 2012). Inside the cells, extra Fe could be maintaining in vacuoles to eschew from stress (Moore et al., 2014). Furthermore, plastids were indicated to have a role in the Fe toxicity tolerance in rice thorough their ability of maintain to 4000 Fe atoms (Briat et al., 2010).
Tanaka, et al. (1966) indicated that the Fe concentration in the culture solution which leads to toxicity of Fe was lower at the vegetative growth stage of rice compared with the later growth stages. Cultural practices such as ridge planting, planting date, pre-submergence of soil and water management could be manipulated to decrease rice Fe toxicity. Using of Fe toxicity tolerant rice cultivars is the most cost effective methods. Therefore, combination of using tolerant cultivar and developed cultural practices can give the great results in high Fe toxicity conditions (Sahrawat et al., 1996; Sahrawat, 2004).
To cope with the constraints posed by different tolerance rankings, a well understanding of the adaptation mechanisms to various Fe toxic environments and the physiological and genetic factors underlying those mechanisms is required rice varieties vary in their iron toxicity tolerance and the screening of rice varieties with better iron tolerance is a momentous component of research for decreasing iron toxicity. Genetic variations in adaptation and tolerance for iron toxicity soil environments have truly been exploited for improving rice varieties with iron toxicity tolerance (Sahrawat ; Sika, 2002; Balasubramanian, et al., 2007; Nozoe, et al., 2008; Sahrawat, 2004, 2010;).
Mechanisms of tolerance were studied in the intolerant (IR29) and the tolerant RIL (FL483) at seedling stage. In shoots, ascorbate oxidase and glutathione-S-transferase genes demonstrated genotypic differences, and FL483 had higher ascorbate oxidase activity and lower dehydroascorbate reductase (Wu et al., 2017). Nayak et al. (2008) with studied 65 genotypes for their iron tolerance in the field indicated that there was a large range in tolerance to iron toxicity and iron tolerant rice genotypes produced higher grain yields than the iron-susceptible cultivars in the respective duration groups (Nayak et al., 2008).
The effort to cope with iron toxicity
Several genetic studies were investigated for Fe toxicity tolerance, such as genes that associated to iron transport including OsIRT (Lee and An, 2009), OsNRAMP1 and OsNRAMP2 (Zhou and Yang, 2004), storage proteins such as ferritin (OsFER) (Stein et al., 2009) and transcription factor such as OsWRKY80 (Ricachenevsky et al., 2010). Several transporters that play role in metal transportation have been recognized in rice (Kobayashi and Nishizawa, 2012).
multiple QTLs were localized at 36.8-41Mb on chromosome 1 (Wu et al., 2014). FL483 is an inbred line that bear the QTLs qFETOX-1-2 and qFETOX-1-1 in this region demonstrated less leaf bronzing notwithstanding similar shoot Fe content with the comparison to IR29 as a sensitive parental line (Wu et al., 2014). Furthermore, genome wide association study carried out by Matthus et al. (2015) using 329 rice accessions. Meaningful markers related to leaf bronzing symptoms identified on chromosomes 1 and 5. The detected loci on chromosome 1 similarity were localized with several QTLs had been previously identified in various studies (Wu et al., 2014; Dufey et al., 2015). Moreover, with a total of 197 QTL have been reported for Fe toxicity in rice, (Wu et al., 1997, 1998; Wan, et al., 2003; Wan, et al., 2005; Shimizu et al., 2005; Ouyang et al., 2007; Fukuda et al., 2012; Zhang, et al., 2013; Wu et al., 2014; Matthus et al., 2015; Dufey et al., 2015, 2009; Liu et al., 2016; Ruengphayak et al., 2015). Four chromosomal regions (CR) have been identified between markers RM246-RM443, RM526- R758, C515-C25 and R1245-RM429 on chromosomal 1, 2, 3 and 7, respectively, that involving in the Fe toxicity tolerance of rice, (Dufey et al., 2015).