Abstract
The plant immune system is equipped with several defensive layers to evade pathogen attack. One of the primary defense includes plasma membrane-localized receptors explicitly detect conserved pathogen-associated molecular patterns. Transcriptional reprogramming of resistant genes confers PAMP-triggered immunity. Consequently basal immunity is triggered which is primarily mediated by several intracellular nucleotide-binding leucine rich repeat receptors. Subsequently, nucleotide-binding leucine rich repeat receptors sense pathogens and activate another defense response known as effector triggered immunity. Both the PTI and ETI are mediated by resistant genes. Interestingly, the detailed molecular function of resistant genes is not yet fully revealed. Resistant genes are also well involved in non pathophysiological conditions such as during cold stress, heat stress, duration of exposure of light and drought stress. Here, we have reported that the Arabidopsis resistant genes AT1G17600, AT4G14368, AT4G16860, AT5G40910 and AT5G45050 are temperature regulated. We found that the transcript levels of AT1G58400, AT2G14080, AT2G17055, AT3G51560, AT4G16950, AT5G40910 and AT5G45050 were significantly raised for the plant samples grown under short-day conditions. The transcript levels of AT1G17600, AT1G27180, AT1G33560, AT2G14080, AT3G51560, AT4G16860 and AT4G16950 were upregulated for plants grown under drought stress conditions. In Arabidopsis, the transcriptional reprogramming is modulated by decapping protein factors. There was no significant change in the protein level of DCPs. Our results suggest that under abiotic stress conditions, the resistant genes differentially express independent of the decapping event.
Highlights
Plant immune response activation is based on precise recognition between a plant receptor and a cognate pathogen effector, famously described as gene-forgene relationship among plant host disease resistant genotypes and avirulent pathogenic strains [1]
It was observed that the resistant genes AT1G17600, AT4G14368 and AT4G16860 are highly expressed when plants are exposed to cold stress (16/8 hr light/dark; 16 °C and 16/8 hr light/dark; 4 °C) relative to their transcript levels under normal physiological growth conditions (16/8 hr light/dark; 22 °C; Fig. 1)
When plants were exposed to heat stress conditions (37 °C; 10 min several resistant genes were expressed at a higher level relative to the transcript levels under normal physiological growth conditions (16/8 hr light/dark; 22 °C)
Summary
Plant immune response activation is based on precise recognition between a plant receptor and a cognate pathogen effector, famously described as gene-forgene relationship among plant host disease resistant genotypes and avirulent pathogenic strains [1]. With the onset of PTI, several other known defense pathways including, reactive oxygen species (ROS) burst, activation of mitogen activated protein kinases (MAPKs), expression of immune related genes is induced in order to prevent non-adapted pathogens from infecting [5]. Another arm of plant immune response, commonly called as effector-triggered immunity (ETI), commonly considered as an amplified version of PTI, is vital for provoking an effective response against pathogenic molecules [6, 7]. Effector molecules are recognized by intracellular nucleotide binding/leucine rich repeat
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