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Details

Autor(en) / Beteiligte
Titel
LEUNIG_HOMOLOG transcriptional co‐repressor mediates aluminium sensitivity through PECTIN METHYLESTERASE46‐modulated root cell wall pectin methylesterification in Arabidopsis
Ist Teil von
  • The Plant journal : for cell and molecular biology, 2017-05, Vol.90 (3), p.491-504
Ort / Verlag
England: Blackwell Publishing Ltd
Erscheinungsjahr
2017
Link zum Volltext
Quelle
Wiley Online Library - AutoHoldings Journals
Beschreibungen/Notizen
  • Summary A major factor determining aluminium (Al) sensitivity in higher plants is the binding of Al to root cell walls. The Al binding capacity of cell walls is closely linked to the extent of pectin methylesterification, as the presence of methyl groups attached to the pectin backbone reduces the net negative charge of this polymer and hence limits Al binding. Despite recent progress in understanding the molecular basis of Al resistance in a wide range of plants, it is not well understood how the methylation status of pectin is mediated in response to Al stress. Here we show in Arabidopsis that mutants lacking the gene LEUNIG_HOMOLOG (LUH), a member of the Groucho‐like family of transcriptional co‐repressor, are less sensitive to Al‐mediated repression of root growth. This phenotype is correlated with increased levels of methylated pectin in the cell walls of luh roots as well as altered expression of cell wall‐related genes. Among the LUH‐repressed genes, PECTIN METHYLESTERASE46 (PME46) was identified as reducing Al binding to cell walls and hence alleviating Al‐induced root growth inhibition by decreasing PME enzyme activity. seuss‐like2 (slk2) mutants responded to Al in a similar way as luh mutants suggesting that a LUH–SLK2 complex represses the expression of PME46. The data are integrated into a model in which it is proposed that PME46 is a major inhibitor of pectin methylesterase activity within root cell walls. Significance Statement Arabidopsis roots respond to Al stress by increasing the cell wall Al binding capacity. This is partly due to decreasing the methylesterification of pectins. The mechanisms involved are not yet understood. We identify LUH as a new modulator of Al sensitivity and PME46 is an inhibitor of PME activity. LUH/SLK2 complex and Al repress PME46 via independent pathways. This leads to lower methylation of cell wall pectins and thus increased Al binding and Al sensitivity.

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