Claim · model-written summary
TCH4 upregulation decreased pectin methylesterification under boron deficiency.
- Taxon
- Arabidopsis
Arabidopsist0 - Treatment
- B-deficient conditionse0
- Gene
- TCH4e0
- Outcome
- degree of methylesterification of pectine0
- Direction
- decreasede0
Not reportedMaterialCompoundOrgan / stageInteractorInteractor roleSecond interactorSecond interactor roleComparatorSettingValueQualifier
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“Up-regulation of TCH4 influenced the ratio of chelator-soluble pectin to alkali-soluble pectin and decreased the degree of methylesterification of pectin under B-deficient conditions”
t0“Arabidopsis”
Title
Cheng Zhang; Mingliang He; Zhexuan Jiang; et al. International Journal of Molecular Sciences 2022. doi:10.3390/ijms23031250
Other claims from this paper (12)
- Intervention effect Boron deficiency induced TCH4 expression.
- Observation TCH4 overexpression lines were more sensitive to boron deficiency than wild-type Col-0.
- Observation TCH4 knockout lines were more resistant to low boron stress than wild-type Col-0.
- Association TCH4 upregulation altered the ratio of chelator-soluble to alkali-soluble pectin under boron deficiency.
- Intervention effect Boron deficiency disturbed cellulose arrangement.
- Intervention effect Boron deficiency enlarged the gap between cellulose microfibrils.
- Intervention effect Boron deficiency decreased cell wall mechanical strength.
- Observation Boron deficiency produced a thickened, deformed triangular cell wall region.
- Observation Cell wall symptoms under boron deficiency were more profound in TCH4 overexpression lines.
- Observation Under boron deficiency, TCH4 overexpression lines had increased O2− content compared with Col-0.
- Observation Under boron deficiency, TCH4 overexpression lines had increased MDA content compared with Col-0.
- Mechanism The authors identify boron deficiency induced TCH4 as a regulator of cell wall homeostasis and plant growth.