Chitosan-induced programmed cell death in plants

Abstract

Chitosan, CN(-), or H(2)O(2) caused the death of epidermal cells (EC) in the epidermis of pea leaves that was detected by monitoring the destruction of cell nuclei; chitosan induced chromatin condensation and marginalization followed by the destruction of EC nuclei and subsequent internucleosomal DNA fragmentation. Chitosan did not affect stoma guard cells (GC). Anaerobic conditions prevented the chitosan-induced destruction of EC nuclei. The antioxidants nitroblue tetrazolium or mannitol suppressed the effects of chitosan, H(2)O(2), or chitosan + H(2)O(2) on EC. H(2)O(2) formation in EC and GC mitochondria that was determined from 2',7'-dichlorofluorescein fluorescence was inhibited by CN(-) and the protonophoric uncoupler carbonyl cyanide m-chlorophenylhydrazone but was stimulated by these agents in GC chloroplasts. The alternative oxidase inhibitors propyl gallate and salicylhydroxamate prevented chitosan- but not CN(-)-induced destruction of EC nuclei; the plasma membrane NADPH oxidase inhibitors diphenylene iodonium and quinacrine abolished chitosan- but not CN(-)-induced destruction of EC nuclei. The mitochondrial protein synthesis inhibitor lincomycin removed the destructive effect of chitosan or H(2)O(2) on EC nuclei. The effect of cycloheximide, an inhibitor of protein synthesis in the cytoplasm, was insignificant; however, it was enhanced if cycloheximide was added in combination with lincomycin. The autophagy inhibitor 3-methyladenine removed the chitosan effect but exerted no influence on the effect of H(2)O(2) as an inducer of EC death. The internucleosome DNA fragmentation in conjunction with the data on the 3-methyladenine effect provides evidence that chitosan induces programmed cell death that follows a combined scenario including apoptosis and autophagy. Based on the results of an inhibitor assay, chitosan-induced EC death involves reactive oxygen species generated by the NADPH oxidase of the plasma membrane.

Chitosan Elicitation for Enhancing of Vincristine and Vinblastine Accumulation in Cell Culture of Catharanthus roseus (L.) G. Don

“…For the chitosan as a stimulant, chitosan is known to elicit activities leading to a variety of defensive responses in host plants to microbial infections, including the accumulation of phytoalexins, pathogen related proteins, callus formation and accumulation of secondary metabolite (Yin et al, 2012). This study found that the most effectivechitosan concentrations for inducing vinblastine and vincristine in C. roseus cell culture were 100 to 250 mg/L because itinduced programmed cell death and hypersensitive-associated responses in plants cell when concentration increased (Vasil'ev et al, 2009) or chitosan toxicity to the living cells or might be due to the phytotoxic action of vinblastine and vincristine on the cells (Amborabé et al, 2008). These results also agreed with the studies in Plumbago indica root cultures of Jaisi and Panichayupakaranant (2016).…”

Induction of auxin biosynthesis and WOX5 repression mediate changes in root development in Arabidopsis exposed to chitosan

“…High doses of this polymer induce peroxidase and polyphenol oxidases, which in turn generate phenolic compounds 3 and calose depositions 52 in plant cells. Chitosan also triggers induction of programed-cell death (PCD) in plants 53 . The involvement of PCD in the inhibitory effect of chitosan on root development should be investigated in future studies.…”

Chitosan in Agriculture: A New Challenge for Managing Plant Disease

“…The most studied plant responses to chitosan treatment are the formation of chemical and mechanical barriers and the synthesis of new molecules and enzymes involved in the defence response [15,37]. In some cases, chitosan causes the induction of the hypersensitive response, mainly around the infection site, that leads to the programmed cell death [44]. This hypersensitive response can be followed by systemic response of the plant defence mechanisms.…”