lators of PCD by specific E3 ligases. Mitochondrial release of cytochrome c via the permeability 24211709 transition pore is repressed at the transcription level Multiple stimuli cause up-regulation of cytochrome c and cytochrome c oxidase expression as early events of PCD. However, during seed ageing, the expression of both genes was down-regulated, and showed a similar trend to that observed in senescing leaves. Increases in cytosolic calcium induce release of cytochrome c from mitochondria through activation of the permeability transition pore, which consists of VDAC and ANT. Up-regulation of VDAC has been reported in plant PCD in response to drought, cold and salicylic acid, Pseudomonas syringae and also during the plant hypersensitive response. In ageing seeds VDAC was down-regulated and the same occurred during leaf senescence, which indicates that VDAC may play a specific role in ageing-induced PCD that differs from PCD triggered by other stresses. ANT was also down-regulated in response to seed ageing. Down regulation of ANT is an early event in the execution phase of PCD induced by heat and senescence and the defence response in Arabidopsis. A decline in ANT protein synthesis may result in a decrease in ATP/ADP exchange, which is one of the 25617690 earliest events of PCD. Other genes that may play a role in the release of pro-apoptotic mitochondrial proteins into the cytosol are aconitases and dihydrolipoyl dehydrogenases, which appear to be particularly susceptible to oxidative stress and were up-regulated in response to seed ageing, indicating a possible involvement in redox signaling to trigger PCD. There have been several reports of a link between carbohydrate metabolism and PCD. For example, glyceraldehyde-3-phosphate dehydrogenase has been linked to PCD in animal cells. GAPDH is inhibited by oxidation of a Cys residue in the active site, which can activate a MAP kinase signalling cascade via a multistep phosphorelay. In addition, disulfide bond formation between GAPDH subunits leads to aggregation, which correlates with the rate of oxidative stress-induced cell death. In this study several glycolytic genes including GAPDH were Seed ageing MedChemExpress HC-067047 causes endoplasmic reticulum stress PCD in animals and plants shares some common phenomena, such as the release of apoptogenic proteins from the mitochondria, induction of caspase-like proteases, and DNA cleavage by PCD-active nucleases to yield multimers of approximately 180bp. In animal cells regulation of the mitochondrial PCD pathway involves proteins of the B-cell lymphoma 2 family e.g. Bax which induces release of cytochrome c from the mitochondria and Bcl-2, which inhibits Bax. Neither protein has been identified in plants, although the heterologous expression of mammalian Bax in A. thaliana and tobacco causes PCD, which is reversed by the over expression of Bax inhibitor-1 . BI-1 is localised in the endoplasmic reticulum, and controls calcium flux into and out of the ER, possibly through interaction with calmodulin. Expression of BI-1 is up-regulated by pathogen inoculation Transcriptome Analysis of Pea Seed Ageing up-regulated. Likewise, Rajjou et al. observed increased levels of GAPDH in a proteomic study of seed ageing, and phosphofructokinase expression was induced during silique wall senescence in Arabidopsis. Both hexokinase and sucrose synthase were upregulated during seed ageing, and induction of sucrose synthase activity was also reported during accelerated ageing of sunflower seeds. Hex