Plant Photo-morphogenesis and Virus Resistance: An important Molecular link
Dharmappa D Chavan* and Halima Khatoon
Advanced Centre of Plant Virology, Division of Plant Pathology, ICAR-Indian Agricultural Research Institute, New Delhi, India
*Corresponding Author: Dharmappa D Chavan, Advanced Centre of Plant Virology, Division of Plant Pathology, ICAR-Indian Agricultural Research Institute, New Delhi, India.
Published: August 07, 2023
Abstract
Both the propagation of plants (Wang et al., 2019) and the transmission of viruses (Paudel and Sanfacon, 2018) are dependent on the presence of light in their environments. When it comes to plants, light is the primary environmental factor that contributes to photosynthesis (Liu et al., 2019) and photomorphogenesis (Montgomery, 2016). According to Paik and Huq (2019), the term "photomorphogenesis" describes a sequence of morphological changes that occur in the development of plants when dark-grown seedlings are exposed to light. A well-known component of light-mediated plant development, the E3 ubiquitin ligase COP1 (Constitutive Photomorphogenesis 1) functions as a repressor of photomorphogenesis. COP1 is also known as Constitutive Photomorphogenesis 1. In this study, we demonstrate that the protein COP1 positively modulates the defence mechanism against the turnip crinkle virus (TCV) and avrRPM1 bacteria by contributing to the stability of the resistance (R) protein HRT and RPM1, respectively. In the context of a cop1 mutant background, both HRT and RPM1 levels, and hence pathogen resistance, are drastically decreased. It is noteworthy that the levels of at least two double-stranded RNA binding (DRB) proteins, DRB1 and DRB4, are reduced in the backdrop of the cop1 mutant, which suggests that COP1 decreases HRT stability via its effect on the DRB proteins. In point of fact, the degradation of HRT was brought about by a mutation in either drb1 or drb4. In contrast to COP1, a multi subunit E3 ligase that was encoded by anaphase-promoting complex (APC) 10 had no effect on DRB1 levels but did negatively affect DRB4 and TCV resistance. Our hypothesis is that the positive control of HRT that is mediated by COP1 is dependent on equilibrium between COP1 and the negative regulators that target DRB1 and DRB4.