Claim · model-written summary
Overexpression of AtMYB2 increases xylem cell numbers.
- Taxon
- Arabidopsis
Arabidopsist0 - Treatment
- Overexpression of AtMYB2e0
- Gene
- AtMYB2e0
- Outcome
- xylem cell numberse0
- Direction
- increasese0
Not reportedMaterialCompoundOrgan / stageInteractorInteractor roleSecond interactorSecond interactor roleComparatorSettingValueQualifier
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
t0“Arabidopsis thaliana”
e0“Overexpression of AtMYB2 decreases cambial cell numbers and increases xylem cell numbers”
Title
Chong Zhang; Xiaorui Guo; Leiqian Sun; et al. Plant Communications 2026. doi:10.1016/j.xplc.2026.101939
Other claims from this paper (13)
- Intervention effect Overexpression of AtMYB2 decreases cambial cell numbers.
- Intervention effect Loss of AtMYB2 results in the opposite phenotype to overexpression.
- Mechanism The authors conclude that AtMYB2 negatively regulates cambial cell proliferation.
- Mechanism The authors conclude that AtMYB2 positively regulates xylem cell differentiation.
- Observation AtMYB48 and AtbHLH68 are direct targets of AtMYB2.
- Mechanism AtMYB48 and AtbHLH68 function as positive regulators of cambial cell proliferation.
- Mechanism AtMYB48 and AtbHLH68 function as negative regulators of xylem differentiation.
- Observation Single mutants of AtMYB48 or AtbHLH68 exhibit only mild phenotypic alterations.
- Observation The atmyb48 atbhlh68 double mutant displays enhanced defects in xylem development.
- Intervention effect Overexpression of either AtMYB48 or AtbHLH68 alone rescues the double mutant phenotype, indicating functional redundancy.
- Observation AtMYB48 and AtbHLH68 can physically interact, but this interaction is dispensable for their regulatory functions in xylem development.
- Observation AtMYB48 primarily regulates genes associated with secondary cell wall deposition and programmed cell death.
- Observation AtbHLH68 predominantly regulates genes involved in cambial cell proliferation.