Salicylate and jasmonate intertwine in ROS-triggered chloroplast-to-nucleus retrograde signaling.

Plants, being sessile, are frequently exposed to environmental perturbations, affecting their sustenance and survival. In response, distinct inherent mechanisms emerged during plant evolution to deal with environmental stresses. Among various organelles, chloroplast plays an indispensable role in plant cells. Besides providing the site for photosynthesis and biosynthesis of many important primary and secondary metabolites, including hormones, chloroplasts also act as environmental sensors. Any environmental perturbation directly influences the photosynthetic electron transport chain, leading to excess accumulation of reactive oxygen species (ROS), causing oxidative damages to biomolecules in the vicinity. To prevent excess ROS accumulation and the consequent oxidative damages, the chloroplast activates retrograde signaling (RS) pathways to reprogramme nuclear gene expression, defining plant's response to stress. Based on levels and site of ROS accumulation, distinct biomolecules are oxidized, generating specific derivatives that act as genuine signaling molecules, triggering specific RS pathways to instigate distinctive responses, including growth inhibition, acclimation, and programmed cell death. Though various RS pathways independently modulate nuclear gene expression, they also implicate the defense hormone salicylic acid (SA) and oxylipins, including 12-oxo-phytodienoic acid (OPDA) and jasmonic acid (JA), by promoting their biosynthesis and utilizing them for intra- and intercellular communications. Several studies reported the involvement of both hormones in individual RS pathways, but the precise dissection of their activation and participation in a given RS pathway remains an enigma. The present review describes the current understanding of how SA and JA intertwine in ROS-triggered RS pathways. We have also emphasized the future perspectives for elucidating stress specificity and spatiotemporal accumulation of respective hormones in a given RS pathway.

Estimating the household secondary attack rate and serial interval of COVID-19 using social media.

We propose a method to estimate the household secondary attack rate (hSAR) of COVID-19 in the United Kingdom based on activity on the social media platform X, formerly known as Twitter. Conventional methods of hSAR estimation are resource intensive, requiring regular contact tracing of COVID-19 cases. Our proposed framework provides a complementary method that does not rely on conventional contact tracing or laboratory involvement, including the collection, processing, and analysis of biological samples. We use a text classifier to identify reports of people tweeting about themselves and/or members of their household having COVID-19 infections. A probabilistic analysis is then performed to estimate the hSAR based on the number of self or household, and self and household tweets of COVID-19 infection. The analysis includes adjustments for a reluctance of Twitter users to tweet about household members, and the possibility that the secondary infection was not acquired within the household. Experimental results for the UK, both monthly and weekly, are reported for the period from January 2020 to February 2022. Our results agree with previously reported hSAR estimates, varying with the primary variants of concern, e.g. delta and omicron. The serial interval (SI) is based on the time between the two tweets that indicate a primary and secondary infection. Experimental results, though larger than the consensus, are qualitatively similar. The estimation of hSAR and SI using social media data constitutes a new tool that may help in characterizing, forecasting and managing outbreaks and pandemics in a faster, affordable, and more efficient manner.