The transmembrane amino acid transporter encoding genes showed a down-regulation in both inoculated and uninoculated old leaves. However, the action of peroxidases and the consequent cell wall lignification may limit the diffusion of these nutrient compounds between the cell and the sub-cuticular space, limiting therefore the fungal growth. Fothergill and Ashcroft showed that V. inaequalis growth was stimulated at pH values above 5.8. Later works suggested a different pH between young and old leaves. With these works it may be suggested that the fungal growth, as a result of sub-optimal growth conditions in old leaves, may be inhibited. In our work, we observed an up-regulation of proton transporter precursor genes in both uninoculated and inoculated old leaves at 72 hpi, while at 96 hpi they were downregulated in both uninoculated and inoculated old leaves. Magnesium ion transmembrane transporter genes did not show any differential expression at 72 hpi and were Lomitapide Mesylate down-regulated in both uninoculated and inoculated old leaves at 96 hpi. Potassium, sodium, chlorine, and calcium ion transporter genes showed a down-regulation in old leaves compared to young ones at both time points. Other unspecified anion transporter genes were down-regulated. However, in the work of Raa and Raa and Overeem, the difference in pH between leaves of different ages was determined with leaf homogenates, which make the assumption of a different pH between young and old leaves difficult to prove with RNA-seq experiments and to connect to V. inaequalis growth. In fact, this pathogen invaded only the subcuticular space of the leaf, thus the acidity of the sub-cuticular space would be a better factor to analyse in future researches. It is characterized clinically by tremor, rigidity, reduced motor activity, and postural instability and pathologically by loss of dopaminergic neurons in the substantia nigra pars compacta and the presence of a-synuclein positive inclusions in the cytoplasm of neurons, termed Lewy bodies. Most cases are idiopathic or late-onset PD, whereas,10% of cases are familial forms. The identification and characterization of genes that cause heritable forms of the disease have provided important insights into the pathways involved in dopaminergic neurodegeneration. Mutations in the Parkin gene represent the most common known cause of early-onset parkinsonism. The Parkin protein is an E3 ubiquitin ligase responsible for the transfer of activated ubiquitin molecules to a protein substrate. This ubiquitination process has various functional consequences in addition to the protein degradation by the 26S proteasome, including regulation of receptor trafficking, cell cycle progression, gene transcription, DNA repair, and immune responses. Studies in Drosophila melanogaster revealed compelling evidence for a role of Parkin in the maintenance of mitochondrial function. Genetic interaction between Parkin and PINK1, mutations of which also cause early-onset Ginsenoside-F4 parkinsonism, indicated that both genes are acting in a common pathway. Loss of one of these two genes results in mitochondrial pathology and muscle and dopaminergic neuron degeneration. Overexpression of Parkin rescues the phenotypes caused by PINK1 deficiency, but not vice versa, indicating that Parkin intervenes downstream of PINK1. In addition, genetic interactions between Parkin and PINK1 and genes encoding components of the mitochondrial fission/ fusion machinery indicate an involvement of the PINK1/Parkin pathway in the regulation of mitochondrial dynamics. Parkin is at steady state essentially cytosolic, and recent work has shown that it selectively and rapidly translocates.