![]() Tight control of MIPS expression seems crucial to regulate MI accumulation and localized cell death on biotic stress.Ĭomplex regulation of MIPS genes has been found in eukaryotes. Interestingly, the transcriptome of mips1 mutants is similar to the one of mpk4 and mkk1/2 mutants, and expression of MIPS1 is reduced in these mutants according to publicly available micro-array data, suggesting that MIPS1 down-regulation may be induced by MAPKs to promote programmed cell death and pathogen resistance. Both mpk4 and mkk1/mkk2 mutants display a dwarf phenotype, spontaneous programmed cell death and constitutive activation of pathogen response. One consisting of MKK4/MKK5 and MPK3/MPK6 appears to activate defense genes, whereas the other comprising MKK1/MKK2 and MPK4 would repress them ( 13 ). Early events of PAMP-induced signaling have been dissected and in the case of bacterial flagellin (flg22), recognition involves two antagonistic MAPK signaling cascades: flagellin recognition by surface receptors triggers the activation of MEKK1, which in turn activates two MAPK modules. Plant defense mechanisms induced by pathogen-associated molecular pattern (PAMP) recognition include hormone signaling via salycilic acid, jasmonic acid and ethylene, regulation of gene expression, strengthening of cell wall reactive oxygen species production and, in some cases, programmed cell death in the case of hypersensitive response ( 12 ). Indeed, mips1 mutants display improved resistance toward Hyaloperonospora arabidopsis, while mips3 mutants are more susceptible to a broad range of pathogens, including viruses, virulent and avirulent bacterial strains and the fungus Botrytis cinerea ( 11 ). Several studies have provided evidence for a role of MIPS in biotic stresses. ![]() Hence, cell fate can be influenced by differential MIPS regulation: its sustained expression is linked to cell proliferation and differentiation, whereas its down-regulation may be involved in the controlled cell death of specific tissues. In plants, cellular suicide is required during many steps of development such as xylogenesis ( 5 ), plant reproduction ( 6 ), leaf and petal senescence ( 7, 8 ) and root cap and endosperm cell death during germination ( 9, 10 ). However, the most striking feature of mips1 mutants is the light-dependent formation of lesions on leaves, implicating MIPS1 as a repressor of programmed cell death ( 2, 3 ). mips1 mutants display pleiotropic defects, including reduced root growth, abnormal vein formation in cotyledons ( 2, 3 ) and defects in auxin polar transport due to alterations in lipid metabolism ( 4 ). The Arabidopsis genome encompasses three isoforms of MIPS, but MIPS1 seems the main player in MI biosynthesis because mips1 mutants have drastically reduced MI content. Loss-of-function studies highlighted the diversity of crucial cellular processes relying on MI. ![]() The rate-limiting step for MI biosynthesis is catalyzed by the MI phosphate synthase (MIPS, E.C.5.5.1.4), and its function has been investigated in various plant species. In plants, products of MI metabolism are involved in diverse processes such as signal transduction, second messenger signaling, stress response, cell wall biogenesis and chromatin remodeling ( 1 ). MI is required for the biosynthesis of a huge variety of cellular components, and thereby plays a crucial role in growth and development. Thus, in plants, MIPS1 appears to have evolved as a protein that connects cellular metabolism, pathogen response and chromatin remodeling.Īlthough it was first isolated from muscles, myo-inositol (MI) is a ubiquitous compound present in all living organisms. Furthermore, on activation of pathogen response, MIPS1 expression is reduced epigenetically, providing evidence for a complex regulatory mechanism acting at the transcriptional level. Here, we demonstrate that MIPS1 binds directly to its promoter to stimulate its own expression by locally inhibiting the spreading of ATXR5/6-dependent heterochromatin marks coming from a transposable element. Surprisingly, we found this enzyme to be imported in the nucleus and to interact with the histone methyltransferases ATXR5 and ATXR6, raising the question of whether MIPS1 has a function in transcriptional regulation. ![]() Because regulation of its activity is instrumental either to support cell proliferation and growth or to promote cell death, the universal myo-inositol phosphate synthase (MIPS), responsible for myo-inositol biosynthesis, is a critical enzyme of primary metabolism.
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