Autophagy-Like Cell Death Regulates Hydrogen Peroxide and Calcium Ion Distribution in Xa3/Xa26-Mediated Resistance to Xanthomonas oryzae pv. oryzae.
Int J Mol Sci
; 21(1)2019 Dec 27.
Article
en En
| MEDLINE
| ID: mdl-31892124
The broad-spectrum and durable resistance gene Xa3/Xa26 against Xanthomonas oryzae pv. oryzae (Xoo) has been widely exploited in rice production in China. But the cytological features of the Xa3/Xa26-mediated resistance reaction have been rarely reported. This study reveals the cytological characteristics of the Xa3/Xa26-mediated resistance reaction against Xoo to uncover the functions of hypersensitive response programmed cell death (HR-PCD) in rice. Autophagy-like cell death, which was characterized by double-membrane bodies appearance in xylem parenchyma cell and mesophyll cell, was inhibited by autophagy inhibitor 3-methyladenin (3-MA). The autophagy-related genes were induced to reach a high level in resistance reaction. The hydrogen peroxide (H2O2) maintained a low concentration on the plasma membrane. The calcium ions localized on the apoplast were transferred into the vacuole. The autophagy inhibitor (3-MA) impaired Xa3/Xa26-mediated resistance by promoting the accumulation of H2O2, and inhibited the transfer of extracellular calcium ions into the vacuole in the xylem parenchyma cells and mesophyll cells. Therefore, the HR-PCD belongs to autophagy-like cell death in the Xa3/Xa26-mediated resistance reaction. These results suggest that the autophagy-like cell death participates in the Xa3/Xa26-mediated resistance by negatively regulating H2O2 accumulation, in order to abolish oxidative stress and possibly activate calcium ion signals in xylem parenchyma cells of the rice leaf.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Proteínas de Plantas
/
Oryza
/
Autofagia
/
Calcio
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Muerte Celular
/
Resistencia a la Enfermedad
/
Peróxido de Hidrógeno
País/Región como asunto:
Asia
Idioma:
En
Revista:
Int J Mol Sci
Año:
2019
Tipo del documento:
Article
País de afiliación:
China