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    Home > Biochemistry News > Microbiology News > [Plant Cell] How do bacteria obtain iron from plants?

    [Plant Cell] How do bacteria obtain iron from plants?

    • Last Update: 2021-03-23
    • Source: Internet
    • Author: User
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    Iron is an essential mineral nutrient element for almost all living organisms.

    Just as animals obtain iron from food, plant pathogens also need to obtain iron from host plants for their own growth and reproduction.

    However, we don't know much about the mechanism of how pathogens obtain iron in plant hosts.

    Pseudomonas syringae (Pst) is a model strain for studying the interaction between the host and the microorganism.
    It can use its three-type secretion system to secrete a variety of effector proteins into plant cells to promote the infection of the pathogen.

    However, the function of most bacterial effector proteins is not fully understood.

    On March 5, 2021, Liu Jun's research group from the Institute of Microbiology of the Chinese Academy of Sciences published a research paper entitled "Bacterial effector targeting of a plant iron sensor facilitates iron acquisition and pathogen colonization" in the international authoritative academic journal The Plant Cell.
    Reveals the molecular mechanism of the effector protein AvrRps4 secreted by bacteria that targets the iron metabolism pathway of plants to obtain iron.

    Jun Liu’s group first analyzed the transcriptome data of 1-24 hours and 8 hours of Arabidopsis wild-type Col-0 and mutant eds after Pst (avrRps4) infection with Pseudomonas syringae Pst (avrRps4), and found a pathway related to plant iron metabolism.
    Many related genes are involved in the response of plants to infection by the pathogen Pst (avrRps4).

    Genetic and biochemical research methods have proved that the effector protein AvrRps4 secreted by the bacteria can target the plant's iron metabolism regulatory protein BTS.

    BTS is the main sensor protein for plants to respond to iron signals and precisely regulate iron homeostasis.

    AvrRps4 can interfere with the degradation of downstream transcription factors bHLH115 and ILR3 by BTS, thereby regulating the iron metabolism process of plants.

    For mutant plants that cannot recognize AvrRps4 (rps4a and eds1-2), the effector protein AvrRps4 can cause the accumulation of total iron in plants and iron in apoplasts.

        However, for those plants that can recognize AvrRps4, the host plant restricts iron absorption through an immune defense response, resulting in less iron accumulation in apoplasts.

    In addition, the important immune components that recognize AvrRps4 (RPS4, EDS1 and RRS1a/b) are also involved in the regulation of iron deficiency in response to BTS.

    These mutant plants (rps4a, eds1-2, and rrs1a/b) showed a phenotype similar to the root length of mutant bts-2 on iron-deficiency medium, indicating that these immune components are also involved in the iron-deficiency response.

    In the process of Pst (avrRps4) infecting plants, BTS is essential for the accumulation of immune response protein EDS1.
    The absence of BTS leads to a decrease in the level of EDS1 in plants, and plants are sensitive to pathogen infection.

    Therefore, this study shows that under the infection of bacteria, the plant immune system tightly regulates the homeostasis of iron in the body, limiting the bacteria's access to a large amount of iron, thereby inhibiting the infection of the bacteria.

    At the same time, the study also revealed the new functions of the pathogenic effector protein and proposed the concept of "iron immunity".

        Xing Yingying, a doctoral graduate of Liu Jun's research group, and Xu Ning, associate researcher, are the co-first authors, and researcher Liu Jun is the corresponding author.

    Thanks to researcher Yu Diqiu of Xishuangbanna Botanical Garden of Chinese Academy of Sciences and researcher Ling Hongqing of Institute of Genetics and Development of Chinese Academy of Sciences for their genetic materials.

    Professor Wang Hongbin from Guangzhou University of Chinese Medicine, Professor Jane Parker from Max Planck Institute in Germany, and Professor Gitta Coaker from University of California, Davis participated in the collaboration.

    This research was funded by the National Natural Science Foundation of China, the Strategic Pilot Project B of the Chinese Academy of Sciences, and the State Key Laboratory of Plant Genomics for this project.

        Original link: https://academic.
    oup.
    com/plcell/advance-article/doi/10.
    1093/plcell/koab075/6159621?guestAccessKey=79142351-31ee-418f-bdae-c9b6e5d3c192  
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