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Summary: Mycoheterotrophic and parasitic plants are heterotrophic and parasitize on fungi and plants, respectively, to obtain nutrients. Large‐scale comparative genomics analysis has not been conducted in mycoheterotrophic or parasitic plants or between these two groups of parasites. We assembled a chromosome‐level genome of the fully mycoheterotrophic plant Gastrodia elata (Orchidaceae) and performed comparative genomic analyses on the genomes of G. elata and four orchids (initial mycoheterotrophs), three parasitic plants (Cuscuta australis, Striga asiatica, and Sapria himalayana), and 36 autotrophs from various angiosperm lineages. It was found that while in the hemiparasite S. asiatica and initial mycoheterotrophic orchids, approximately 4–5% of the conserved orthogroups were lost, the fully heterotrophic G. elata and C. australis both lost approximately 10% of the conserved orthogroups, indicating that increased heterotrophy is positively associated with gene loss. Importantly, many genes that are essential for autotrophs, including those involved in photosynthesis, the circadian clock, flowering time regulation, immunity, nutrient uptake, and root and leaf development, were convergently lost in both G. elata and C. australis. The high‐quality genome of G. elata will facilitate future studies on the physiology, ecology, and evolution of mycoheterotrophic plants, and our findings highlight the critical role of gene loss in the evolution of plants with heterotrophic lifestyles. Significance Statement: Mycoheterotrophic and parasitic plants are very special as they parasitize fungi and plants, respectively, to obtain nutrients. We sequenced the genome of the fully mycoheterotrophic orchid Gastrodia elata, which is achlorophyllous and leaf‐ and rootless, and compared it with the genome of the obligate parasite Cuscuta australis. We found that G. elata and C. australis similarly but independently lost many genes important for normal autotrophic plants to adapt to heterotrophic lifestyles. [ABSTRACT FROM AUTHOR]

Anaesthesia exposure causes changes in the developing brain and affects behaviour and memory. This study examined the beneficial effect of pachypodol against isoflurane (ISF)‐induced neuronal injury. Seven‐day‐old rats were treated with 10 mg/kg and 30 mg/kg intravenous pachypodol 30 min before exposure to ISF (0.75%) for 6 h. Oxidative stress and other biochemical parameters were assessed in the brain tissue and serum using enzyme‐linked immunosorbent assay. Additionally, a terminal deoxynucleotidyl transferase dUTP nick‐end labelling (TUNEL) assay was performed to assess neuronal cell apoptosis in several regions of the hippocampus. Cognitive function and neurological scores were determined in the pachypodol‐treated neuron‐injured rats. Cytokine levels and oxidative stress were reduced in the pachypodol‐treated group compared with the ISF group. In addition, cognitive deterioration was reversed in pachypodol‐treated compared with ISF‐treated rats. Thus, treatment with pachypodol reduced neuronal apoptosis in neuron‐injured rats. Moreover, pachypodol ameliorated changes to the JNK/ERK/Akt pathway in brain‐injured rats. In conclusion, pachypodol treatment prevents neuronal apoptosis in ISF‐treated rats by regulating the JNK/ERK pathway. [ABSTRACT FROM AUTHOR]

Abstract: Atmospheric CO2 levels are rapidly increasing due to human activities. However, the effects of elevated CO2 (ECO2) on plant defense against insects and the underlying mechanisms remain poorly understood. Here we show that ECO2 increased the photosynthetic rates and the biomass of tobacco and rice plants, and the chewing lepidopteran insects Spodoptera litura and Mythimna separata gained less and more mass on tobacco and rice plants, respectively. Consistently, under ECO2, the levels of jasmonic acid (JA), the main phytohormone controlling plant defense against these lepidopteran insects, as well as the main defense‐related metabolites, were increased and decreased in insect‐damaged tobacco and rice plants. Importantly, bioassays and quantification of defense‐related metabolites in tobacco and rice silenced in JA biosynthesis and perception indicate that ECO2 changes plant resistance mainly by affecting the JA pathway. We further demonstrate that the defensive metabolites, but not total N or protein, are the main factors contributing to the altered defense levels under ECO2. This study illustrates that ECO2 changes the interplay between plants and insects, and we propose that crops should be studied for their resistance to the major pests under ECO2 to predict the impact of ECO2 on future agroecosystems. [ABSTRACT FROM AUTHOR]

Summary A dodder (Cuscuta) often simultaneously parasitizes two or more adjacent hosts. Phosphate (Pi) deficiency is a common stress for plants, and plants often interact with soil microbes, including arbuscular mycorrhizal fungi (AMF), to cope with Pi stress. Little is known about whether dodder transmits Pi deficiency‐induced systemic signals between different hosts. In this study, dodder‐connected plant clusters, each composed of two tobacco (Nicotiana tabacum) plants connected by a dodder, were established, and in each cluster, one of the two tobacco plants was treated with Pi starvation. AMF colonization efficiency, rhizosphere bacterial community, and transcriptome were analyzed in the other dodder‐connected Pi‐replete tobacco plant to study the functions of interplant Pi signals. We found that dodder transfers Pi starvation‐induced systemic signals between host plants, resulting in enhanced AMF colonization, changes of rhizosphere bacterial communities, and alteration of transcriptomes in the roots of Pi‐replete plants. Importantly, genetic analyses indicated that microRNA399s (miR399s) and strigolactones suppress the systemic Pi signals and negatively affect AMF colonization in the Pi‐replete plants. These findings provide new insight into the ecological role of dodder in mediating host–host and host–microbe interactions and highlight the importance of strigolactone and miR399 pathways in systemic Pi signaling. [ABSTRACT FROM AUTHOR]