Myo-Inositol Metabolism and Stress Tolerance in Plants

Myo-inositol occupies a central position in plant biochemistry as both a metabolic precursor and a signalling hub. Synthesised from glucose-6-phosphate by myo-inositol-1-phosphate synthase (MIPS), it gives rise to a family of derivatives that includes phosphoinositides, galactinol and phytic acid. These compounds underpin membrane biogenesis, vesicular trafficking and osmotic adjustment, and modulate hormonal networks governing salicylic acid and ethylene responses. Under salinity or drought, elevated myo-inositol and its oligomers act as compatible solutes, stabilising proteins and membranes. In immunity and programmed cell death, nuclear and cytosolic pools of inositol derivatives integrate reactive oxygen species signals to fine-tune defence gene expression. Genetic manipulation of MIPS alleles has demonstrated marked improvements in salt tolerance, reactive oxygen scavenging and delayed senescence, highlighting myo-inositol metabolism as a versatile target for crop resilience enhancement. Continued elucidation of biosynthetic regulation and interconnection with hormone pathways promises new strategies to bolster global agricultural productivity under mounting environmental pressures.

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Myo-Inositol Metabolism and Stress Tolerance in Plants publication trend

The graph below shows the total number of articles in myo-inositol metabolism and stress tolerance in plants across all publications each year (not limited to Nature Index journals).

Technical terms

Myo-Inositol: A cyclic six-carbon polyol serving as precursor to inositol phosphates, phosphoinositides and osmoprotective oligosaccharides.

Myo-Inositol-1-Phosphate Synthase (MIPS): The enzyme catalysing the NAD⁺-dependent cyclisation of glucose-6-phosphate to inositol-1-phosphate, committing flux into inositol metabolism.

Reactive Oxygen Species (ROS): Highly reactive oxygen-containing molecules that act as signalling agents in stress responses but can damage cells at elevated levels.

Programmed Cell Death (PCD): A genetically regulated process of cellular suicide essential for development and defence against pathogens.

Salicylic Acid (SA): A phenolic plant hormone central to local and systemic defence signalling and modulation of programmed cell death.

Ethylene: A gaseous plant hormone that regulates senescence, stress responses and cell-death processes, often interacting with inositol-derived signals.

References

1. Crosstalks between Myo-Inositol Metabolism, Programmed Cell Death and Basal Immunity in Arabidopsis. PLOS ONE (2009).
2. A Novel Salt-tolerant l-myo-Inositol-1-phosphate Synthase from Porteresia coarctata (Roxb.) Tateoka, a Halophytic Wild Rice MOLECULAR CLONING, BACTERIAL OVEREXPRESSION, CHARACTERIZATION, AND FUNCTIONAL INTROGRESSION INTO TOBACCO-CONFERRING SALT TOLERANCE PHENOTYPE*. Journal of Biological Chemistry (2004).
3. Myo-inositol mediates reactive oxygen species-induced programmed cell death via salicylic acid-dependent and ethylene-dependent pathways in apple. Horticulture Research (2020).