Autotoxin Rg1 Induces Degradation of Root Cell Walls and Aggravates Root Rot by Modifying the Rhizospheric Microbiome.

Management of crop root rot disease is one of the key factors in ensuring sustainable development in agricultural production. The accumulation of autotoxins and pathogens in soil has been reported as a primary driver of root rot diseases; however, less is known about the correlation of plants, their associated pathogens and microbiome mediated by autotoxins as well as the contributions autotoxins make to the occurrence of root rot disease. Here, we integrated metabolomic, transcriptomic, and rhizosphere microbiome analyses to identify the root cell wall degradants cellobiose and d-galacturonic acid as being induced by the autotoxic ginsenoside Rg1 of Panax notoginseng, and we found that exogenous cellobiose and d-galacturonic acid in addition to Rg1 could aggravate root rot disease by modifying the rhizosphere microbiome. Microorganisms that correlated positively with root rot disease were enriched and those that correlated negatively were suppressed by exogenous cellobiose, d-galacturonic acid, and Rg1. In particular, they promoted the growth and infection of the soilborne pathogen Ilyonectria destructans by upregulating pathogenicity-related genes. Cellobiose showed the highest ability to modify the microbiome and enhance pathogenicity, followed by Rg1 and then d-galacturonic acid. Collectively, autotoxins damaged root systems to release a series of cell wall degradants, some of which modified the rhizosphere microbiome so that the host plant became more susceptible to root rot disease. IMPORTANCE The accumulation of autotoxins and pathogens in soil has been reported as a primary driver of root rot disease and one of the key factors limiting sustainable development in agricultural production. However, less is known about the correlation of plants, their associated pathogens, and the microbiome mediated by autotoxins, as well as the contributions autotoxins make to the occurrence of root rot disease. In our study, we found that autotoxins can damage root systems, thus releasing a series of cell wall degradants, and both autotoxins and the cell wall degradants they induce could aggravate root rot disease by reassembling the rhizosphere microbiome, resulting in the enrichment of pathogens and microorganisms positively related to the disease but the suppression of beneficial microorganisms. Deciphering this mechanism among plants, their associated pathogens, and the microbiome mediated by autotoxins will advance our fundamental knowledge of and ability to degrade autotoxins or employ microbiome to alleviate root rot disease in agricultural systems.

Current Iodine Nutrition Status and Morbidity of Thyroid Nodules in Mainland China in the Past 20 Years.

The aim of this study was to comprehensively assess the prevalence of goiter and thyroid nodules (TNs) in relation to China's iodine nutrition level over the past 20 years and provide an effective reference for developing health policies. PubMed, EMBASE, Chinese National Knowledge Infrastructure, Chongqing VIP, and Chinese Wan Fang databases were searched for relevant studies from Jan 1996 to Feb 2020. Two reviewers extracted valid data from the eligible citations to determine the morbidity of TNs in different urinary iodine concentrations (UICs) and in patients of different genders, of different ages, who live in different geographic regions, and who live at different altitudes, as well as the P values of interactions between groups. There were 26 articles (34 studies) included in this analysis. The overall morbidity of TNs in mainland China was 23.4%. Morbidity was higher in urban areas (P < 0.001) than in rural and mixed areas. Coastal areas (P < 0.001), female patients (P < 0.001), high-altitude areas (P < 0.001), and residence in south China (P < 0.001) were all associated with higher morbidity of TNs. The lowest morbidity value of TNs, 16%, was in the more-than-adequate iodine subgroup. The highest morbidity, 27.2%, was in the adequate iodine subgroup. The morbidity of TNs increases with age, and women are more likely to have TNs. We also need to perform more epidemiological studies, and in the future, we should cultivate better understanding of the relationship between other thyroid diseases and provide more comprehensive and useful information for other researchers.

Panax notoginseng Root Cell Death Caused by the Autotoxic Ginsenoside Rg1 Is Due to Over-Accumulation of ROS, as Revealed by Transcriptomic and Cellular Approaches.

Panax notoginseng is a highly valuable medicinal herb, but its culture is strongly hindered by replant failure, mainly due to autotoxicity. Deciphering the response mechanisms of plants to autotoxins is critical for overcoming the observed autotoxicity. Here, we elucidated the response of P. notoginseng to the autotoxic ginsenoside Rg1 via transcriptomic and cellular approaches. Cellular analyses demonstrated that Rg1 inhibited root growth by disrupting the cell membrane and wall. Transcriptomic analyses confirmed that genes related to the cell membrane, cell wall decomposition and reactive oxygen species (ROS) metabolism were up-regulated by Rg1 stress. Further cellular analyses revealed that Rg1 induced ROS ([Formula: see text] and H2O2) accumulation in root cells by suppressing ascorbate peroxidase (APX) and the activities of enzymes involved in the ascorbate-glutathione (ASC-GSH) cycle. Exogenous antioxidants (ASC and gentiobiose) helped cells scavenge over-accumulated ROS by promoting superoxide dismutase (SOD) activity and the ASC-GSH cycle. Collectively, the autotoxin Rg1 caused root cell death by inducing the over-accumulation of ROS, and the use of exogenous antioxidants could represent a strategy for overcoming autotoxicity.

Autotoxic ginsenosides in the rhizosphere contribute to the replant failure of Panax notoginseng.

BACKGROUND AND AIMS: Sanqi ginseng (Panax notoginseng) growth is often hampered by replant failure. In this study, we aimed to examine the role of autotoxicity in Sanqi replant failures and assess the role of ginsenosides in autotoxicity. METHODS: The autotoxicities were measured using seedling emergence bioassays and root cell vigor staining. The ginsenosides in the roots, soils, and root exudates were identified with HPLC-MS. RESULTS: The seedling emergence and survival rate decreased significantly with the continuous number of planting years from one to three years. The root exudates, root extracts, and extracts from consecutively cultivated soils also showed significant autotoxicity against seedling emergence and growth. Ginsenosides, including R1, Rg1, Re, Rb1, Rb3, Rg2, and Rd, were identified in the roots and consecutively cultivated soil. The ginsenosides, Rg1, Re, Rg2, and Rd, were identified in the root exudates. Furthermore, the ginsenosides, R1, Rg1, Re, Rg2, and Rd, caused autotoxicity against seedling emergence and growth and root cell vigor at a concentration of 1.0 µg/mL. CONCLUSION: Our results demonstrated that autotoxicity results in replant failure of Sanqi ginseng. While Sanqi ginseng consecutively cultivated, some ginsenosides can accumulate in rhizosphere soils through root exudates or root decomposition, which impedes seedling emergence and growth.