The lack of nitric oxide production in Al treated roots also causes the production of jasmonic acid, a hormone-like molecule in plants known to regulate environmental stresses such as ozone, heavy metals and pathogen attack . Determination of Al-induced toxicity is further complicated by interference with mineral absorption at the root apex, resulting in deficiency symptoms in plants grown on Al toxic soils. This is particularly true for the divalent cations Ca2+, Mg2+, and K+ as well as PO4-3 . Al has been found to competitively inhibit uptake of Ca2+, Mg2+ and K+ and the addition of these cations to the soil can ameliorate the toxic effects of Al . Impairment of ion uptake occurs via blockage of ion channels in the plasma membrane and is likely the cause of the interruption of intracellular Ca2+ and Mg2+ homeostasis and the rapid depolarization of the plasma membrane following Al exposure . In response to the cellular damage caused by internalization of Al, plants must activate signal transduction pathways in order to cope with the onslaught of stress caused by Al. It is well documented that Al induces transcriptional programs in order to facilitate detoxification and redistribution of Al within the plant body. For example, ALS3 is an Al-inducible gene that encodes an ABC-like transporter proposed to redistribute Al away from the most Al sensitive tissues such as the root apical meristem in order to maintain root growth . Other Arabidopsis genes that are Al inducible have a protective role, such as ALMT1, an Alinducible malate transporter that exudes malate as an Al-chelator,round flower buckets as well as genes those involved in oxidative stress responses such as AtBCB , peroxidases, glutathione-S-transferases, and superoxide dismutase .

Overexpression of several of these types of genes in Arabidopsis reduces Al toxicity symptoms in conjunction with lowering Aldependent oxidative damage . Another well-documented hallmark of Al-inducible response is rapid deposition of callose in the plasmodesmata, or junctions in cell wall that allow interconnections between cells, which can be observed in plants within a few hours of treatment with Al . Callose is a β-1,3-glucan that is normally found very rarely within plant cells and only known to be involved in a few specific developmental processes, such as pollen tube growth and as part of pprotein plugs in sieve tube elements in response to wounding. Callose deposition in plasmodesmata is a regulated response to stress, likely to isolate affected or damaged cells from healthy ones. Because deposition of callose is so tightly linked to Al exposure, callose accumulation has been a useful marker for assessing manifestation of Al toxicity in cells of the root tip . These Al-inducible responses represent just a few processes that are related to the hundreds of genes that have been found to be upregulated following Al exposure . As of now, it has been nearly impossible to differentiate between those genes that are of central importance to Al toxicity and stoppage of root growth and those that encode peripheral secondary factors that are only tangentially related. Determining whether various factors are related to the primary or secondary effects of Al-dependent root growth inhibition has proven to be a great challenge to understanding the nature of Al toxicity and the molecular basis of Al-dependent stoppage of root growth, although recent results suggest that Al-dependent DNA damage may be of paramount importance.Responses to the toxic effects of Al soils have been extensively documented for a wide range of plant species.

As discussed, Al exposure has been found to impede cell division and cell elongation, nutrient uptake, hormone signaling, cytoskeletal structure, Ca2+ homeostasis, plasma membrane integrity, inhibition of ATP requiring enzymatic reactions that depend on an Mg-ATP complexes, and interference caused by Al binding anionic targets within the cell . Plants have adopted two distinctly different strategies for preventing Al-dependent growth inhibition. Exclusion of Al from roots, considered to be an Al resistance mechanism, is an effective and simple strategy for increasing root growth in an Al toxic environment largely because Al does not come into contact with its biochemical targets. Al exclusion is a distinctly different mechanism from true Al tolerance, in which roots cope with internalized Al. The study of Al tolerance has generally been considered to be an intractable problem largely because of the complexity of Al toxicity as discussed, with the expectation being that changes in any one target of Al would have little positive impact on growth due to the sheer number of biochemical targets of Al. Clearly, an effective and straightforward strategy for increasing root growth in Al toxic environments is Al exclusion, where plants prevent the internalization of Al. Certainly, based on the predicted complexity of Al-binding sites once it enters the cellular environment, prevention of Al uptake is by far the simplest approach for reducing Al toxicity. Release of Al-chelating organic acids has been documented as the primary Al resistance mechanism in multiple plant species including wheat, maize, and barley. Organic acids excreted from roots chelate Al in the rhizosphere to form nontoxic complexes that in some way prevent Al uptake. By not internalizing Al, the root tip is protected from Al-related damage that can be severe enough to cause terminal differentiation of the quiescent center in the root apical meristem .

Al chelation commonly occurs through exudation of malate, citrate, or oxalate to render Al insoluble . Paradoxically, it has been argued that in animal systems, an Al-citrate complex is the form that is most readily transported across a cellular membrane, thus making it unclear as to why such complexes prevent internalization in plants . Regardless, besides preventing internalization into the symplast, these organic acid-Al complexes also reduce the capability of Alto directly interact with the negative charges of the apoplast such as polygalacturonic acids and other components of the cell wall like pectin, which would normally increase wall rigidity and cause gross physical damage upon cell elongation . Organic acid-dependent Al exclusion was first reported in Al resistant snapbean cultivars and subsequently studied intensively in an Al resistant wheat cultivar that has roots that secrete malic acid into the rhizosphere in response to Al . Following characterization of the role of the wheat Alt1 locus in Al exclusion, it was found that the Al resistance associated with it was dependent on increased expression levels of ALMT1, plastic flower buckets wholesale which encodes an Al-activated root malate efflux transporter that has subsequently been reported in several plant species . In Al resistant species, there are a variety of genes that have been characterized that are required for Al resistance. It has been determined that usually one or a small handful of these genes are required to confer Al resistance to these plants. This was first identified in an Al resistant wheat cultivar where the roots secrete the organic acid malate into the rhizosphere to chelate Al after exposure . Since then, a number of other plant species have been found to employ a similar technique such as malate release by Arabidopsis; citrate release by maize, oat, snapbean, sorghum and soybean; buckwheat and taro release oxalate; oat, radish, rapeseed and rye release both citrate and malate . Organic acids are also released from the root apex, as it is the primary site of Al-dependent root growth inhibition, but not from the mature root region . Of the three organic acids that are secreted from the root apex, citrate is the most common and forms the most stable and nontoxic complex with Al since it forms a 1:1 ratio with Al. Oxalate and malate both have less affinity for Al since they are both divalent anions . The Al-induced secretion of organic acids can be classified into two patterns depending on the plant species. In Pattern I plants such as Al-tolerant wheat and buckwheat, there is no delay between Al exposure and release of organic acids into the rhizosphere. This pattern suggests that the transporter is not induced by gene activation. There are a variety of proposed mechanisms on how this occurs: direct interaction with channel proteins, direct interaction with specific receptors on the membrane that activates secondary messengers to change the channel activity, or enters the cytoplasm and alters the channel activity either directly or indirectly .

In contrast, Pattern II plants such as Cassia tora, rye and triticale have a delayed response to Al, signifying that gene induction may be involved. This pattern probably involves activation of genes that might be related to the metabolism of organic acids, the anion channel on the plasma membrane or transport of organic acids from the mitochondria. Also this pattern is only observed for the secretion of citrate . Research on organic acid secretion has identified specific transporters and mechanisms that are responsible for the export of organic acids into the rhizosphere. The first Al induced gene responsible for organic ion efflux transport was found in wheat, Aluminum Activated Malate Transporter . This transporter exports malate and when it is over expressed can confer Al tolerance to tobacco cells and also barley, which is one of the most Al sensitive cereal crops. Additionally, over-expressing ALMT1 in barley conferred increased resistance to Al in both a hydroponic culture and in acidic soils . Expression of ALMT1 in tobacco cells showed recovery beginning 18 hours after Al exposure. Since the characterization of wheat ALMT1, several active organic acid transporters have been identified such as: Arabidopsis AtALMT1, sorghum AltSB, and barley HvAACT1 . While ALMT1 and AtALMT1 are novel proteins, the citrate transporter in barley is a member of the multidrug and toxic compound extrusion family . This suggests that there could be other, unidentified genes that are encoding anion channels that are important for Al-tolerance . There are other compounds that are capable of chelating Al in plants, although they have not been well characterized. Of these compounds, phenolics have been receiving more attention in relation to Al tolerance due to their ability to complex with metals and act as strong antioxidants in response to abiotic stress . Phenolics, characterized as organic compounds that have one or more aromatic ring, are released from maize roots, such as catechin and quercetin. In three different wild type maize genotypes, it was shown that the release of these compounds had a better correlation between the ability of Altolerance than with Al-activated oxalate release. Likely, Al-stimulated release of phenolics may play an important role in the detoxification of Al at the root tip . Chelation of Al as a mechanism of preventing root damage is not limited to the release of organic acids and phenolics into the rhizosphere, since the same mechanism is used to detoxify internalized Al. In Al-tolerant species such as hydrangea, buckwheat, and tea, Al is chelated, internalized and transported as a non-toxic species within the plant. The two extensively studied plant species that utilize this method are hydrangea and buckwheat. When hydrangea is grown in the presence of Al, its sepals change color from red to blue due to the accumulation of the blue colored Al complex. The Al-citrate complex is an incredibly strong complex. Using NMR, it was found that the Al-citrate complex is more stable than the Al-ATP complex suggesting that this complex can protect cellular components from the damaging effects of Al . In buckwheat, it was found that the plant secretes oxalic acid from the root apex, where it forms a 1:3 Al-oxalate complex. The Al-oxalate complex is then transported through the xylem sap from the roots to the leaves. The 1:3 Al-oxalate complex is also very strong, and also has a higher stability constant that is much higher than Al-ATP, meaning that it also can prevent Al binding to cellular components . Further research also shows that the Al-oxalate complex in leaves of buckwheat is sequestered to the vacuoles, which may be an additional detoxification step . Furthermore, in tea it has been proposed that Al is transported through the roots to the shoots as an Al-citrate complex , where Al accumulates at the cell walls of epidermal cells . By creating complexes with TCA intermediates, these plants can accumulate high concentrations of Al, which represents one mechanism of true Al tolerance. Transcriptional activation of Al tolerance genes like ALMT1 and ALS3 are mediated by STOP1 and STOP2, putative transcription factors responsible for the upregulation of a suit of genes necessary for Al tolerance .