Claim · model-written summary
Loss of function of SnRK1α1 restores autophagy, free amino acid and TOR pathway activity levels in CYTc-deficient plants.
- Taxon
- plantsViridiplantaee5
- Treatment
- loss-of-function of the gene encoding the SnRK1α1 subunite5
- Outcome
- autophagy, free amino acid and TOR pathway activity levelse6
- Direction
- restorese5
- Comparator
- CYTc-deficient plantse5
Not reportedMaterialGeneCompoundOrgan / stageInteractorInteractor roleSecond interactorSecond interactor roleSettingValueQualifier
Verbatim
e5“loss-of-function of the gene encoding the SnRK1α1 subunit restores the growth of CYTc-deficient plants”
e6“as well as autophagy, free amino acid and TOR pathway activity levels, which are affected in these plants”
Title
Florencia P. Coronel; Diana E. Gras; M. Victoria Canal; et al. The Plant Journal 2024. doi:10.1111/tpj.17215
Other claims from this paper (9)
- Intervention effect Plants with reduced CYTc show impaired growth.
- Intervention effect Plants with reduced CYTc show increased global expression of stress-responsive genes.
- Intervention effect CYTc-deficient plants show activation of the SnRK1 pathway.
- Intervention effect The carbohydrate levels of CYTc-deficient plants are not significantly different from wild-type.
- Intervention effect Loss of function of the SnRK1α1 gene restores the growth of CYTc-deficient plants.
- Intervention effect Increasing CYTc levels decreases SnRK1 pathway activation, reflected in reduced SnRK1α1 phosphorylation.
- Intervention effect Increasing CYTc levels did not change total SnRK1α1 protein levels.
- Intervention effect Under mannitol stress, the growth of CYTc-deficient plants is relatively less affected than that of wild-type plants.
- Mechanism SnRK1 function is affected by CYTc levels.