The cell wall is crucial for cellular sensitivity to low pH: the role of class III peroxidases and ethylene in cell death in Arabidopsis thaliana roots

• Ano de defesa: 2018
• Autor(a) principal: Graças, Jonathas Pereira das
• Tipo de documento: Tese
• Tipo de acesso: Acesso aberto
• Idioma: eng
• Instituição de defesa: Biblioteca Digitais de Teses e Dissertações da USP
• Palavras-chave em Português: Acidez; Acidity; Cell death; Cell wall integrity; Cell wall tension; Class III peroxidases; Ethylene; Etileno; Integridade de parede celular; Morte celular; Peroxidases de classe III; Tensão de parede celular
• Link de acesso: http://www.teses.usp.br/teses/disponiveis/11/11144/tde-25072018-164614/

Evidence suggests that root cell walls are a target of low pH stress. Severe low pH stress causes cell death in the root tip. The walls of these cells are highly dynamic. Our hypothesis is that in these cells low pH causes stress in the cell wall due to excessive loosening. Thus, a certain level of turgor pressure should be required to cause cell death. Here, we aimed to investigate the role of the cell wall in low pH stress leading to cell death. We looked for the possible involvement of players such as class III peroxidases and ethylene signaling, which could promote changes in the cell wall and cause differential sensitivity to low pH. Arabidopsis thaliana and mutants in the genetic background of Col-0 were grown in a medium containing agar (0.8%) and half the concentration of Hoagland\'s nutrient medium. Five-day-old seedlings were exposed to low pH in a solution composed of 0.5 mM CaCl2 and 0.6 mM Homopipes buffer. Treatment of roots at pH 4.6 caused death of cells in the transition zone (TZ) and meristematic zone (MZ). However, cell death was negligible when plants were treated at pH 4.6 in an hyperosmotic solution (Ψs = -0.37 MPa), thereby decreasing cell wall tension. Also, an hypoosmotic treatment (HO) caused cell death at pH 5.8 in TZ. Cell death was accelerated when HO was performed in a low pH solution. The mutant of a cell wall integrity sensor protein, wak-1, displayed reduced cell death when exposed to low pH. Also, cell death seems to occur through a programmed cell death mechanism. Thus, low-pH induced cell death appears to be triggered by perception of cell wall stress. We examined published data to search for class III peroxidases possibly involved in cell death due to low pH. The gene for AtPrx62 is induced 8.37-fold in low pH exposed roots. The atprx62 KO mutant was less sensitive to low pH than Col-0 roots. The mRNA of AtPRX62 accumulated in the same zone that cell death occurred due to low pH. This strongly suggests that AtPRX62 is positive regulator of low-pH induced cell death. Also, ethylene pretreatment induced subsequent tolerance of roots to low pH and this was dependent of its receptor ETR1. Together we show that a cell wall stress caused by low pH causes cell death. This death was in part due AtPRX62 activity and was also suppressed by ethylene.