Tropical and arctic ecosystems are largely under sampled. Moreover, the PFT-based root distributions have not been updated accordingly. A global-scale maximum rooting depth data set was synthesized by Canadell et al. [1996] and included 253 plant species. They also aggregated maximum rooting depth data based on PFTs, which is readily applicable to large-scale land models. The rooting depth followed the order: forest > shrub > herbaceous plants > – crops. However, within-PFT variation was quite large. For example, the maximum rooting depth of tropical species was 68 m, while the mean of tropical evergreen plant maximum rooting depth was about 15 m. Particularly for arctic tundra, a more detailed rooting depth data set was developed by Iversen et al. [2015a]. Tundra maximum rooting depth ranged from 0.7 cm for a deciduous shrub species to 100 cm for a forb species . In general, evergreen shrub tundra has the shallowest rooting depth . Grass, forb, and deciduous shrub tundra have deeper root systems , and sedge tundra has the deepest roots . This data set casts doubt on land model PFT classifications for arctic tundra. For example, CLM and ALM represent arctic tundra with only two PFTs , which substantially under represents root traits across the wide range of dominant tundra species, including arctic grasses, sedges, forbs, deciduous shrubs,nft hydroponic and evergreen shrubs [Chapin et al., 1996].The ability of plants to recognize and respond to the presence of threats is vital for their survival. Given their sessile lifestyle this defense response must be swift.

Major threats to plants include diseases caused by microbial phytopathogens. Evolution has duly equipped plants, resulting in plant disease being the exception, not the rule . However, due to extensive selective breeding and the tendency of farmers to plant monocultures, plant disease has gained a foothold and has become a multibillion dollar problem . Currently, the solution is the application of pesticides which are often not only toxic to pathogens but can affect non-target plant and animal species . The off-target effects of pesticides make the discovery of novel solutions to the plant disease problem crucial . In plants, many physical and chemical barriers exist that passively prevent pathogen infection. Physical barriers can include: a waxy cuticle, stomata, and thick cell walls. Chemical barriers include phytoanticipins, phenolics, and quinines which have antimicrobial properties, as well as lactones, cyanogenic glucosides, saponins, terpenoids, stilbenes and tannins . While passive defenses are effective against some phytopathogens, an active immune system is required to combat pathogens able to bypass passive immunity . One such form of active defense includes small basic peptides called plant defensins . PDFs can interfere with a pathogen’s ability to extract nutrients, thus delaying pathogen development . Plant-pathogen interactions are dynamic and shaped by a ‘coevolutionary arms race’ . In this arms race, there are strong selective pressures for the plant to maintain its resistance against a given pathogen, as well as pressures on pathogens to overcome plant defenses . Like mammalian organisms, plants possess an inducible innate immune system that is based on the genetically determined and inheritable recognition of molecular features of pathogens .

Unlike mammals, however, plants do not have specialized immune cells and most plant cell types are capable of efficient innate immune responses. In addition to local innate immunity acting in plant tissues subject to pathogen attack, mobile signals generated in such primary infection sites control systemic defense responses mediating long lasting broad spectrum disease resistance. This innate immune system is constantly evolving in a fashion described by the ‘zigzag model’ . According to this model, the most fundamental form of plant innate immunity involves recognition of conserved molecular signatures shared by many classes of pathogens termed microbe-associated molecular patterns . MAMPs are recognized by pattern-recognition receptors on the surface of plant cells. MAMPs are essential for a pathogen survival and fitness and cannot be discarded or altered through evolution to evade PRRmediated detection . Examples of MAMPs include: chitin and ergosterol from fungi, β-glucans from oomycetes, fungal xylanase and oomycete transglutaminase, as well as flagellin and lipopolysaccharides from gram-negative bacteria . Upon recognition of a MAMP, the plant activates a comprehensive set of defense reactions called pattern-triggered immunity . During PTI there are extensive molecular, morphological, and physiological changes . Signaling cascades link recognition and response. Within minutes of MAMP recognition, there are ion fluxes across the plasma membrane, an increase in cytosolic Ca2+, an oxidative burst, which includes the production of reactive oxygen species and nitric oxide, MAP kinase activation, protein phosphorylation, and receptor endocytosis . Protein kinases are major regulators of plant defense responses that act at various hierarchical levels within the defense network . There are more than 1000 protein kinases in the plant model organismArabidopsis thaliana . In particular, receptor protein kinases , Ca2+ dependent protein kinases and MAPKs have been extensively implicated in the regulation of plant immune responses. The plant immune responses are controlled by a complex regulatory network consisting of multiple interconnected sectors that include those regulated by salicylic acid – and others dependent on jasmonic acid and ethylene as well as other less well characterized pathways .

Over time, pathogens evolved effector molecules which are released to augment virulence by manipulating and weakening, PTI resulting in effector triggered susceptibility . Such interactions between virulent pathogens and susceptible plants are termed “compatible”. A susceptible plant still maintains low levels of defense, called basal defense. Basal defense is not sufficient to fully prevent disease, but it can slow its progression . PTI is often successful against pathogens that have not evolved the ability to specifically infect a plant; this is referred to as non-host resistance. To counteract ETS, plants evolved resistance proteins , which specifically recognize pathogen effectors resulting in a resistant plant and an avirulent pathogen . This type of innate immunity is referred to as effector-triggered immunity . ETI is a faster and more robust version of PTI,nft system and often results in a hypersensitive response at the site of infection . HR involves a programmed form of death of plant cells directly in contact with an invading pathogen. In some cases pathogens evolved additional effectors to evade ETI . ETI is active against adapted pathogens. Although, these relationships are not always set in stone and they may depend on the specific elicitor molecules present during pathogen infection .This means that they can recognize pathogen effectors if tge effects of the effector on the host target. A strong oxidative burst and HR cell death are considered hallmarks for resistance mediated via R genes. ROIs have antimicrobial properties and act as a signal for activation of defense responses, including HR . HR cell death is an efficient immune response against biotrophic pathogens . Biotrophic pathogens extract their food from living plant tissue, while necrotrophs kill and digest dead plant tissue for their nutrients. Thus, by decreasing the number of cells in contact with an invading biotrophic pathogen, plants can prevent further infection. Basal defense and some cases of ETI are controlled by the SA-dependent branch of the defense network . The molecular changes that occur after pathogen recognition during ETI also occur during compatible interactions, but with ‘slower kinetics and reduced amplitude’ . SA-dependent signaling processes involve several genetically defined defense regulators, such as EDS1 and PAD4 , which control the synthesis and accumulation of this defense hormone. Defense associated SA appears to be mainly synthesized by a plastidic pathway that involves isochorismate synthase 1, which is also known as EDS16 or SID2 .

Elevated SA levels activate a set of downstream defense responses, such as expression of pathogenesis-related genes and HR cell death . A positive feedback loop links ROI, NO and SA . These signaling molecules mutually control their production. Only strong activation of this feedback loop results in the induction of HR cell death . Typically levels of ROI, NO and SA accumulation during basal defense are too low to trigger HR . Sifficiently high levels of these signaling molecules for HR induction are typically observed during ETI . SA is also a critical signal for the activation of systemic acquired resistance , a broad-spectrum defense response that is sometimes activated throughout the entire plant in response to local recognition of either virulent or avirulent pathogens . The main role of SA in SAR induction seems to be in the systemic tissue, where it causes the transcriptional co-activator NPR1 to move from the cytoplasm to the nucleus where it interacts with transcription factors, activating SAR . The SA-derivative, methyl salicylate , acts in tobacco as a long-distance mobile signal for SAR within the plant . In addition, MeSA can also serve as the airborne signal that induces defense gene expression in neighboring plants . Recent studies have revealed that SAR can increase the fitness of pathogen-challenged plants in a field setting . Although constitutive activation of SAR has substantial fitness costs . R proteins do not confer resistance against necrotrophic pathogens, which kill plants and feed off dead host tissue. Defense against necrotrophic pathogens is mediated through the jasmonate acid and ethylene branches of the defense network. The JA/ET branches are also known to have roles in responses to wounding and herbivore attack . The SA, JA, and ET pathways interact extensively. A large body of research has indicated that SA and JA are mutually inhibitory . Recent evidence indicates that they may enhance each other’s expression at low concentrations . A plant must be able to distinguish between different types of pathogens allowing it to respond with an appropriate set of defense reactions, mediated by signaling molecules. Thus, different signaling mechanisms are required to activate immune responses against pathogens with different life-styles. Studies indicate that while sometimes ET and JA interact synergistically in disease responses, that both can act independently or even antagonistically with the SA-dependent pathway . Resistance to specific pathogens conferred through JA signaling show little overlap in transcriptional changes. This context is important to fine-tuning the JA response . ET and abscisic acid regulate different branches of the JA response . JA and ET act together to induce the expression of PDF1.2 . The transcription factors, ERF1 and ORA59 work to integrate JA and ET signaling . These transcription factors confer resistance against necrotrophs . Alternately, MYC2 works with ABA signaling to negatively regulate the JA-ET responsive branch while activating genes within its own branch, such as VSP2 . This branch is associated with the wound response and priming for pathogen defense .Arabidopsis and the oomycete, Hyaloperonospora arabidopsidis , are an effective model pathosystem in which defined R-genes mediate recognition of certain Hpa isolates . Well characterized Arabidopsis mutants allow for the fine dissection of defense pathways . While useful, traditional genetics techniques are unable to circumvent functional redundancy and lethal phenotypes. This suggests that additional experimental approaches are necessary to advance knowledge of mechanisms controlling plant immunity. Chemical genetics/genomics offers distinct advantages over traditional techniques through the use of small molecules, whose effects are often impermanent and reversible. Small molecules also provide more defined temporal control. In contrast, the timing of pathogen infections is not easily defined, as the germination of spores or pathogen growth and spread in plants is often asynchronous.As discussed above, different plant species have developed effective mechanisms to cope with pathogens. Unfortunately, contemporary crops have lost parts of their innate immune system due to breeding efforts focused mainly on increasing yield. Consequently, plant diseases cause dramatic losses in crops every year. In the United States 500 million kg of pesticides are applied annually at a cost of $10 billion to farmers to control disease. Despite this, more than a third of all food crops are still destroyed by diseases . The lingering residues of pesticides on produce is currently a major health concern of consumers . Many pesticides currently in use are carcinogenic and rely on direct anti-pathogenic activity, which often leads to undesirable side effects that can have far reaching consequences both for humans and the environment . This disquiet over the dangers of pesticides has spawned considerable interest in alternative methods of disease control .