Plants live under different biotic and abiotic stress conditions, and, to cope with the adversity and severity, plants have well-developed resistance mechanisms. The mechanism starts with perception of the stimuli followed by molecular, biochemical, and physiological adaptive measures. The family of LRR-RLKs (leucine-rich repeat receptor-like kinases) is one such group that perceives biotic and abiotic stimuli and also plays important roles in different biological processes of development. This has been mostly studied in the model plant, Arabidopsis thaliana, and to some extent in other plants, such as Solanum lycopersicum, Nicotiana benthamiana, Brassica napus, Oryza sativa, Triticum aestivum, Hordeum vulgare, Brachypodium distachyon, Medicago truncatula, Gossypium barbadense, Phaseolus vulgaris, Solanum tuberosum, and Malus robusta. Most LRR-RLKs tend to form different combinations of LRR-RLKs-complexes (dimer, trimer, and tetramers), and some of them were observed as important receptors in immune responses, cell death, and plant development processes. However, less is known about the function(s) of LRR-RLKs in response to abiotic and biotic stresses. Here, we give recent updates about LRR-RLK receptors, specifically focusing on their involvement in biotic and abiotic stresses in the model plant, A. thaliana. Furthermore, the recent studies on LRR-RLKs that are homologous in other plants is also reviewed in relation to their role in triggering stress response processes against biotic and abiotic stimuli and/or in exploring their additional function(s). Furthermore, we present the interactions and combinations among LRR-RLK receptors that have been confirmed through experiments. Moreover, based on GENEINVESTIGATOR microarray database analysis, we predict some potential LRR-RLK genes involved in certain biotic and abiotic stresses whose function and mechanism may be explored.

The identification and understanding of metabolic pathways is a key aspect in crop improvement and drug design. The common approach for their detection is based on gene annotation and ontology. Correlation-based network analysis, where metabolites are arranged into network formation, is used as a complentary tool. Here, we demonstrate the detection of metabolic pathways based on correlation-based network analysis combined with machine-learning techniques. Metabolites of known tomato pathways, non-tomato pathways, and random sets of metabolites were mapped as subgraphs onto metabolite correlation networks of the tomato pericarp. Network features were computed for each subgraph, generating a machine-learning model. The model predicted the presence of the β-alanine-degradation-I, tryptophan-degradation-VII-via-indole-3-pyruvate (yet unknown to plants), the β-alanine-biosynthesis-III, and the melibiose-degradation pathway, although melibiose was not part of the networks. In vivo assays validated the presence of the melibiose-degradation pathway. For the remaining pathways only some of the genes encoding regulatory enzymes were detected.

The nitrogen (N)-rich ureides allantoin and allantoate, which are products of purine catabolism, play a role in N delivery in Leguminosae. Here, we examined their role as an N source in nonlegume plants using Arabidopsis (Arabidopsis thaliana) plants mutated in XANTHINE DEHYDROGENASE1 (AtXDH1), a catalytic bottleneck in purine catabolism. Older leaves of the Atxdh1 mutant exhibited early senescence, lower soluble protein, and lower organic N levels as compared with wild-type older leaves when grown with 1 mm nitrate but were comparable to the wild type under 5 mm nitrate. Similar nitrate-dependent senescence phenotypes were evident in the older leaves of allantoinase (Ataln) and allantoate amidohydrolase (Ataah) mutants, which also are impaired in purine catabolism. Under low-nitrate conditions, xanthine accumulated in older leaves of Atxdh1, whereas allantoin accumulated in both older and younger leaves of Ataln but not in wild-type leaves, indicating the remobilization of xanthine-degraded products from older to younger leaves. Supporting this notion, ureide transporter expression was enhanced in older leaves of the wild type in low-nitrate as compared with high-nitrate conditions. Elevated transcripts and proteins of AtXDH and AtAAH were detected in low-nitrate-grown wild-type plants, indicating regulation at protein and transcript levels. The higher nitrate reductase activity in Atxdh1 leaves compared with wild-type leaves indicated a need for nitrate assimilation products. Together, these results indicate that the absence of remobilized purine-degraded N from older leaves of Atxdh1 caused senescence symptoms, a result of higher chloroplastic protein degradation in older leaves of low-nitrate-grown plants.

Sulfite reductase (SiR) is an essential enzyme of the sulfate assimilation reductive pathway, which catalyzes the reduction of sulfite to sulfide. Here, we show that tomato (Solanum lycopersicum) plants with impaired SiR expression due to RNA interference (SIR Ri) developed early leaf senescence. The visual chlorophyll degradation in leaves of SIR Ri mutants was accompanied by a reduction of maximal quantum yield, as well as accumulation of hydrogen peroxide and malondialdehyde, a product of lipid peroxidation. Interestingly, messenger RNA transcripts and proteins involved in chlorophyll breakdown in the chloroplasts were found to be enhanced in the mutants, while transcripts and their plastidic proteins, functioning in photosystem II, were reduced in these mutants compared with wild-type leaves. As a consequence of SiR impairment, the levels of sulfite, sulfate, and thiosulfate were higher and glutathione levels were lower compared with the wild type. Unexpectedly, in a futile attempt to compensate for the low glutathione, the activity of adenosine-5′-phosphosulfate reductase was enhanced, leading to further sulfite accumulation in SIR Ri plants. Increased sulfite oxidation to sulfate and incorporation of sulfite into sulfoquinovosyl diacylglycerols were not sufficient to maintain low basal sulfite levels, resulting in accumulative leaf damage in mutant leaves. Our results indicate that, in addition to its biosynthetic role, SiR plays an important role in prevention of premature senescence. The higher sulfite is likely the main reason for the initiation of chlorophyll degradation, while the lower glutathione as well as the higher hydrogen peroxide and malondialdehyde additionally contribute to premature senescence in mutant leaves.