Gasotransmitter H2S accelerates seed germination via activating AOX mediated cyanide-resistant respiration pathway

Hydrogen sulfide (H2S) has been witnessed as a crucial gasotransmitter involving in various physiological processes in plants. H2S signaling has been reported to involve in regulating seed germination, but the underlying mechanism remains poorly understood. Here, we found that endogenous H2S production was activated in germinating Arabidopsis seeds, correlating with upregulated both the transcription and the activity of enzymes (LCD and DES1) responsible for H2S production. Moreover, NaHS (the H2S donor) fumigation significantly accelerated seed germination, while H2S-generation defective (lcd/des1) seeds exhibited decreased germination speed. Further results indicated that the alternative oxidase (AOX), a cyanide-insensitive terminal oxidase, can be stimulated by imbibition, and the expression of AOX genes was provoked lag behind H2S production during germination. Additionally, exogenous H2S fumigation significantly reinforced imbibition induced enhancement of AOX1A expression, and mediated post-translational modification to keep AOX in its reduced and active state, which mainly involved H2S induced increase of the GSH/GSSG ratio and the cell reducing power. Consequently, H2S signaling acts as a trigger to induce AOX mediated cyanide-resistant respiration to accelerate seed germination. Our study correlates H2S signaling to cyanide metabolism, which also participates in endogenous H2S generation, providing evidence for more extensive studies of H2S signaling.

Jasmonic Acid- and Ethylene-Induced Mitochondrial Alternative Oxidase Stimulates Marssonina brunnea Defense in Poplar

Mitochondrial processes are implicated in plant response to biotic stress caused by viruses, actinomyces, bacteria and pests, but their function in defense against fungal invasion remains unclear. Here, we investigated the role and regulation of mitochondrial alternative oxidase (AOX) in response to black spot disease caused by the hemibiotrophic fungus Marssonina brunnea in poplar. M. brunnea inoculation induced the transcription of the AOX1a gene in the mitochondrial electron transport chain and of jasmonic acid (JA) and ethylene (ET) biosynthetic genes, with the accumulation of these phytohormones in poplar leaf, while inhibiting the transcript amount of the mitochondrial cytochrome c oxidase gene (COX6b) and genes related to salicylic acid (SA). Enhanced AOX reduced poplar susceptibility to M. brunnea with a higher ATP/ADP ratio while the repressed AOX caused the reverse effect. Exogenous JA and 1-aminocyclopropane-1-carboxylic acid (ACC, a biosynthetic precursor of ET) inhibited the transcript amount of COX6b and consequently increased the ratio of AOX pathway to total respiration. Furthermore, the transcription of CYS C1 and CYS D1 genes catalyzing cyanide metabolism was induced, while the cysteine (CYS) substrate levels reduced upon M. brunnea inoculation; exogenous JA and ACC mimicked the effect of M. brunnea infection on cysteine. Exogenous SA enhanced, while JA and ACC reduced, poplar susceptibility to M. brunnea. Moreover, inhibiting AOX completely prohibited JA- and ET-increased tolerance to M. brunnea in poplar. These observations indicate that the JA- and ET-induced mitochondrial AOX pathway triggers defense against M. brunnea in poplar. This effect probably involves cyanide. These findings deepen our understanding of plant–pathogenic fungi interactions.

Histo- and cytopathology of trunk phloem necrosis, a form of rubber tree (Hevea brasiliensis Müll. Arg.) tapping panel dryness

Trunk phloem necrosis (TPN) is a physiological disease of rubber tree (Hevea brasiliensis Müll. Arg.) discovered in the 1980s. It has been distinguished from rubber tree tapping panel dryness (TPD) by its macroscopic symptoms and presumed origin. But little attention has been paid to its microscopic features, and there is now some evidence that both syndromes could be linked to an impaired cyanide metabolism. In order to characterise TPN and compare it with TPD microscopically, the inner phloem of tapping panels was investigated by light and transmission electron microscopy in healthy trees and TPN-affected trees. TPN-affected phloem presented numerous and varied structural and ultrastructural features. There were signs of cellular deterioration in a great number of specialised cells, i.e. laticifers and sieve tubes, and not very specialised cells, i.e. parenchyma cells and companion cells. There were also signs of cellular dedifferentiation in other parenchymatous cells, e.g. in tylosoids and hyperplasic cells. These cells were derived from parenchyma cells that ensheath laticifers in which the latex coagulated. Numerous structural features of TPN are common to TPD, notably tylosoids associated with in situ coagulated latex, which are also known to be early structural markers of TPD and cyanide-induced. It is therefore concluded that TPN is identical to or a variant of TPD, and is a degenerative disease of rubber tree trunk phloem resembling plant stress response, programmed cell death and plant tumourigenesis in some aspects.