High impact information on MOR1

• RIC1-dependent microtubule organization not only locally inhibits outgrowth but in turn suppresses ROP2 activation in the indentation zones [1].
• Point mutations that substitute single amino-acid residues in an amino-terminal HEAT repeat impart reversible temperature-dependent cortical microtubule disruption, showing that MOR1 is essential for cortical microtubule organization [2].
• MOR1 is a member of the MAP215 family of microtubule-associated proteins and is required to establish interphase arrays of cortical microtubules in plant cells [3].
• Phenotypic analysis of gem1-1 and gem1-2, which contains a T-DNA insertion, confirm that MOR1/GEM1 is essential for regular patterns of cytokinesis [3].
• Here, we show that itb1 mutants display cell expansion defects similar to those reported for the distorted class of trichome mutants, including disruption of actin and microtubule organization [4].

Biological context of MOR1

• To determine whether MOR1 functions generally in cytokinesis, we examined the ultrastructure of cell division in roots of the original mor1-1 allele [5].
• The rid5 phenotype was found to result from a mutation in the MOR1/GEM1 gene encoding a microtubule-associated protein [6].
• TMBP200, a microtubule bundling polypeptide isolated from telophase tobacco BY-2 cells is a MOR1 homologue [7].
• MICROTUBULE ORGANIZATION 1 regulates structure and function of microtubule arrays during mitosis and cytokinesis in the Arabidopsis root [8].
• Prior studies with the temperature-sensitive mor1 mutants of Arabidopsis (Arabidopsis thaliana), which harbor single amino acid substitutions in an N-terminal HEAT repeat, proved that MOR1 regulates cortical microtubule organization and function [8].

Anatomical context of MOR1

• The independence of cortical microtubule organization and cellulose microfibril alignment was supported by the observation that double mutants of mor1-1 and rsw1-1, the cellulose-deficient mutant with misaligned microfibrils, had additive phenotypes [9].
• The fra1 mutation did not cause any defects in cell wall composition, secondary wall thickening, or cortical microtubule organization in fiber cells [10].
• In addition, oryzalin and colchicine, which disrupt the microtubule organization, stimulated and stabilized calcium channel activities in wild-type but remained ineffective on ton 2 protoplasts [11].
• During plant cytokinesis, kinesin-related motor proteins are believed to play critical roles in microtubule organization and vesicle transport in the phragmoplast [12].

Associations of MOR1 with chemical compounds

• The original mutant mor1 alleles were reported to have disrupted cortical microtubules, swollen organs and normal cytokinesis, whereas other alleles, embryo-lethal gemini pollen 1 (gem1), have defective pollen cytokinesis [5].
• At the restrictive temperature of mor1-1, root expansion was hypersensitive to the microfilament-disrupting drugs latrunculin B and cytochalasin D, while immunofluorescence microscopy showed that low doses of latrunculin B exacerbated microtubule disruption [13].

Other interactions of MOR1

• A semidominant mutation in an Arabidopsis mitogen-activated protein kinase phosphatase-like gene compromises cortical microtubule organization [14].
• These include the Arabidopsis HINKEL protein and NACK1 and two from tobacco (Nishihama et al., 2002), which are involved in microtubule organization during mitotic cytokinesis [15].
• Indirect immunofluorescence of alpha-tubulin revealed that very few microtubules were present in mutant cells, resulting in the total lack of the parallel microtubule organization that is typical of elongating cells in the wild type [16].
• Microtubule organization is partly disrupted in the spiral1 mutant of Arabidopsis thaliana, which displays a right-handed helical growth phenotype in rapidly elongating epidermal cells [17].

References