Remodeling of the major light-harvesting antenna protein of psii protects the young leaves of barley (Hordeum vulgare L.) from photoinhibition under prolonged iron deficiency

Akihiro Saito, Tomohisa Iino, Kintake Sonoike, Eitaro Miwa, Kyoko Higuchi

    Research output: Contribution to journalArticle

    17 Citations (Scopus)

    Abstract

    Because of the high demand for iron of the photosynthetic apparatus in thylakoid membranes, iron deficiency primarily affects the electron transfer between the two photosystems (PSI and PSII), resulting in photooxidative damage in plants. However, in barley, PSII is protected against photoinhibition, and the plant survives even with a low iron content in its chlorotic leaves. In this study, we report an adaptation mechanism of the photosynthetic apparatus in barley to iron deficiency, which is concomitant with the remodeling of a PSII antenna system. Transcriptome analysis revealed that long-term iron deficiency induced the expression of two genes of the major light-harvesting Chl a/b-binding protein of PSII (LHCII), namely HvLhcb1.11 and HvLhcb1.12 . Chl fluorescence analysis of the wild type and Lhcb1-less chlorina mutants clearly showed that non-photochemical quenching (NPQ) of the wild type was increased by approximately 200 % by iron deficiency, whereas NPQ of chlorina mutants did not change significantly under iron deficiency. The mutant showed severe photodamage in young leaves under prolonged iron deficiency, suggesting that the HvLhcb1 protein is essential for both thermal dissipation and photoprotection in iron-deficient barley. Analysis of thylakoid protein complexes revealed that the proportion of the monomeric form of Lhcb1 significantly increased in barley grown under iron-deficient conditions. We hypothesize that alteration of the HvLhcb1 subpopulations modifies the organization of LHCII in the thylakoid membranes, which is a key step for thermal dissipation to compensate for excess excitation energy and thereby protect the photosystems from serious damage in iron-deficient barley leaves.

    Original languageEnglish
    Pages (from-to)2013-2030
    Number of pages18
    JournalPlant and Cell Physiology
    Volume51
    Issue number12
    DOIs
    Publication statusPublished - 2010 Dec

    Fingerprint

    light harvesting complex
    photoinhibition
    Hordeum
    Hordeum vulgare
    Iron
    barley
    iron
    Light
    leaves
    Proteins
    Thylakoids
    thylakoids
    mutants
    Hot Temperature
    heat
    photostability
    Gene Expression Profiling
    plant damage
    major genes
    transcriptomics

    Keywords

    • Barley (Hordeum vulgare)
    • Iron deficiency
    • Lhcb1
    • Non-photochemical quenching
    • PAM
    • Rice (Oryza sativa)

    ASJC Scopus subject areas

    • Plant Science
    • Physiology
    • Cell Biology

    Cite this

    Remodeling of the major light-harvesting antenna protein of psii protects the young leaves of barley (Hordeum vulgare L.) from photoinhibition under prolonged iron deficiency. / Saito, Akihiro; Iino, Tomohisa; Sonoike, Kintake; Miwa, Eitaro; Higuchi, Kyoko.

    In: Plant and Cell Physiology, Vol. 51, No. 12, 12.2010, p. 2013-2030.

    Research output: Contribution to journalArticle

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    abstract = "Because of the high demand for iron of the photosynthetic apparatus in thylakoid membranes, iron deficiency primarily affects the electron transfer between the two photosystems (PSI and PSII), resulting in photooxidative damage in plants. However, in barley, PSII is protected against photoinhibition, and the plant survives even with a low iron content in its chlorotic leaves. In this study, we report an adaptation mechanism of the photosynthetic apparatus in barley to iron deficiency, which is concomitant with the remodeling of a PSII antenna system. Transcriptome analysis revealed that long-term iron deficiency induced the expression of two genes of the major light-harvesting Chl a/b-binding protein of PSII (LHCII), namely HvLhcb1.11 and HvLhcb1.12 . Chl fluorescence analysis of the wild type and Lhcb1-less chlorina mutants clearly showed that non-photochemical quenching (NPQ) of the wild type was increased by approximately 200 {\%} by iron deficiency, whereas NPQ of chlorina mutants did not change significantly under iron deficiency. The mutant showed severe photodamage in young leaves under prolonged iron deficiency, suggesting that the HvLhcb1 protein is essential for both thermal dissipation and photoprotection in iron-deficient barley. Analysis of thylakoid protein complexes revealed that the proportion of the monomeric form of Lhcb1 significantly increased in barley grown under iron-deficient conditions. We hypothesize that alteration of the HvLhcb1 subpopulations modifies the organization of LHCII in the thylakoid membranes, which is a key step for thermal dissipation to compensate for excess excitation energy and thereby protect the photosystems from serious damage in iron-deficient barley leaves.",
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    AU - Saito, Akihiro

    AU - Iino, Tomohisa

    AU - Sonoike, Kintake

    AU - Miwa, Eitaro

    AU - Higuchi, Kyoko

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    AB - Because of the high demand for iron of the photosynthetic apparatus in thylakoid membranes, iron deficiency primarily affects the electron transfer between the two photosystems (PSI and PSII), resulting in photooxidative damage in plants. However, in barley, PSII is protected against photoinhibition, and the plant survives even with a low iron content in its chlorotic leaves. In this study, we report an adaptation mechanism of the photosynthetic apparatus in barley to iron deficiency, which is concomitant with the remodeling of a PSII antenna system. Transcriptome analysis revealed that long-term iron deficiency induced the expression of two genes of the major light-harvesting Chl a/b-binding protein of PSII (LHCII), namely HvLhcb1.11 and HvLhcb1.12 . Chl fluorescence analysis of the wild type and Lhcb1-less chlorina mutants clearly showed that non-photochemical quenching (NPQ) of the wild type was increased by approximately 200 % by iron deficiency, whereas NPQ of chlorina mutants did not change significantly under iron deficiency. The mutant showed severe photodamage in young leaves under prolonged iron deficiency, suggesting that the HvLhcb1 protein is essential for both thermal dissipation and photoprotection in iron-deficient barley. Analysis of thylakoid protein complexes revealed that the proportion of the monomeric form of Lhcb1 significantly increased in barley grown under iron-deficient conditions. We hypothesize that alteration of the HvLhcb1 subpopulations modifies the organization of LHCII in the thylakoid membranes, which is a key step for thermal dissipation to compensate for excess excitation energy and thereby protect the photosystems from serious damage in iron-deficient barley leaves.

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