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SUMMARY: Lesion‐mimic mutants (LMMs) serve as valuable resources for uncovering the molecular mechanisms that govern programmed cell death (PCD) in plants. Despite extensive research, the regulatory mechanisms of PCD and lesion formation in various LMMs remain to be fully elucidated. In this study, we identified a rice LMM named early leaf lesion and senescence 1 (els1), cloned the causal gene through map‐based cloning, and confirmed its function through complementation. ELS1 encodes an anthranilate synthase α‐subunit involved in anthranilate biosynthesis. It is predominantly localized in chloroplasts and is primarily expressed in light‐exposed tissues. Mutation of ELS1 triggers upregulation of its homologous gene, ASA1, via a genetic compensation response, leading to the activation of the tryptophan (Trp) synthesis pathway and amino acid metabolism. The accumulation of abnormal Trp‐derived intermediate metabolites results in reactive oxygen species (ROS) production and abnormal PCD in the els1 mutant, ultimately causing the leaf lesion phenotype. The els1 mutant also exhibits reduced chlorophyll content, upregulation of genes related to chloroplast degradation and leaf senescence, and decreased activity of photosynthetic proteins, indicating that ELS1 plays a role in chloroplast development. These factors collectively contribute to the premature leaf senescence observed in the els1 mutant. Our findings shed light on the role of ELS1 in regulating ROS accumulation and PCD in rice, providing further genetic insights into the molecular mechanisms governing leaf lesions and senescence. Significance Statement: This study identifies a novel lesion‐mimic mutant in rice, els1, caused by a mutation in the anthranilate synthase α‐subunit. The findings reveal the critical role of ELS1 in regulating reactive oxygen species (ROS) balance and programmed cell death (PCD), offering new insights into the genetic mechanisms controlling leaf senescence and lesion formation in plants. [ABSTRACT FROM AUTHOR]

When developing strategies aimed at mitigating air pollution in densely populated urban areas, it is vital to accurately investigate the vertical distribution of airborne particulate matter (PM) and its primary influencing factors. For this study, field experiments were conducted to quantify the vertical distribution and dispersion processes of PM at five vertical heights related to trees—including at street level near vehicular emission sources (0.3 m), pedestrian breathing height (1.5 m), beneath the canopy (6 m), mid-canopy (9 m), and the top of the canopy (12 m)—within a street-facing building in Wuhan, China. Comparing the vertical dispersion patterns of PM with six particle sizes (PM1, PM2.5, PM4, PM7, PM10, and total suspended particulates—TSPs), larger particles exhibited more pronounced variations with height, notably TSPs (correlation coefficient of −0.95) and PM10 (−0.84). The findings consistently revealed a downward trend in PM concentrations across various particle sizes with increasing height, indicating a negative linear correlation between particle concentrations and altitude within the street canyon. For every 1% increase in vertical height, the PM2.5 concentration decreased by approximately 5.44%, the PM10 concentration decreased by 132.1%, and the TSP concentration decreased by 180.6%. These findings show potential for guiding building designers in developing effective strategies, such as optimal vent placement, in order to mitigate the intrusion of outdoor air pollution—particularly PM2.5—into indoor environments. Furthermore, this research provides novel insights for residents living in street-facing buildings and individuals with respiratory diseases, aiding them in the selection of residential floors to minimize health risks associated with exposure to respirable PM. [ABSTRACT FROM AUTHOR]

Calcium (Ca2+) is a versatile intracellular second messenger that regulates several signaling pathways involved in growth, development, stress tolerance, and immune response in plants. Autoinhibited Ca2+-ATPases (ACAs) play an important role in the regulation of cellular Ca2+ homeostasis. Here, we systematically analyzed the putative OsACA family members in rice, and according to the phylogenetic tree of OsACAs, OsACA9 was clustered into a separated branch in which its homologous gene in Arabidopsis thaliana was reported to be involved in defense response. When the OsACA9 gene was knocked out by CRISPR/Cas9, significant accumulation of reactive oxygen species (ROS) was detected in the mutant lines. Meanwhile, the OsACA9 knock out lines showed enhanced disease resistance to both rice bacterial blight (BB) and bacterial leaf streak (BLS). In addition, compared to the wild-type (WT), the mutant lines displayed an early leaf senescence phenotype, and the agronomy traits of their plant height, panicle length, and grain yield were significantly decreased. Transcriptome analysis by RNA-Seq showed that the differentially expressed genes (DEGs) between WT and the Osaca9 mutant were mainly enriched in basal immune pathways and antibacterial metabolite synthesis pathways. Among them, multiple genes related to rice disease resistance, receptor-like cytoplasmic kinases (RLCKs) and cell wall-associated kinases (WAKs) genes were upregulated. Our results suggest that the Ca2+-ATPase OsACA9 may trigger oxidative burst in response to various pathogens and synergically regulate disease resistance and leaf senescence in rice. [ABSTRACT FROM AUTHOR]