The heteropolymer lignin represents an untapped resource for production of renewable aromatic chemicals, if efficient depolymerisation methods can be developed. In this work, the metabolic pathways in Rhodococcus jostii RHA1 for degradation of aromatic lignin breakdown products are re-routed, in order to generate an aromatic dicarboxylic acid product that could be used for bioplastic synthesis. Protocatechuic acid is normally metabolised via ortho-cleavage to the -keto-adipate pathway. Insertion of recombinant genes for protocatechuate 4,5-dioxygenase or protocatechuate 2,3-dioxygenase into R. jostii RHA1, followed by ammonia cyclisation of the extradiol cleavage products, generates pyridine 2,4-dicarboxylic acid or pyridine 2,5-dicarboxylic acid bioproducts in yields of 80-125 mg/L when grown on minimal media containing 1% wheat straw lignocellulose.

The activation of N-Methyl D-Aspartate Receptor (NMDAR) by glutamate is crucial in the nervous system function, particularly in memory and learning. NMDAR is composed by two GluN1 and two GluN2 subunits. GluN2B has been reported to participate in the prevalent NMDAR subtype at synapses, the GluN1/2A/2B. Here we studied the regulation of GluN2B expression in cortical neurons finding that glutamate up-regulates GluN2B translation through the action of nitric oxide (NO), which induces the phosphorylation of the eukaryotic translation initiation factor 2 α (eIF2α). It is a process mediated by the NO-heme-regulated eIF2α kinase (HRI), as the effect was avoided when a specific HRI inhibitor or a HRI small interfering RNA (siHRI) were used. We found that the expressed GluN2B co-localizes with PSD-95 at the postsynaptic ending, which strengthen the physiological relevance of the proposed mechanism. Moreover the receptors bearing GluN2B subunits upon NO stimulation are functional as high Ca2+ entry was measured and increases the co-localization between GluN2B and GluN1 subunits. In addition, the injection of the specific HRI inhibitor in mice produces a decrease in memory retrieval as tested by the Novel Object Recognition performance. Summarizing our data suggests that glutamatergic stimulation induces HRI activation by NO to trigger GluN2B expression and this process would be relevant to maintain postsynaptic activity in cortical neurons.