Lack of endoplasmic reticulum quality control (ERQC) promotes tonoplast (TP) targeting of KORRIGAN 1 (KOR1).
Yukihiro NagashimaZeyang MaXiuren ZhangAntje von SchaewenHisashi KoiwaPublished in: Plant signaling & behavior (2020)
Cellular dynamics of KORRIGAN 1 (KOR1) is closely linked with cellulose biosynthesis and plant osmotic stress tolerance. Cycling of KOR1 between the plasma membrane (PM) and trans-Golgi Network (TGN) is maintained by sequence motifs and protein structures that are recognized by cellular transport and quality control mechanisms. Several mutations in KOR1, as well as in the host genetic background, promote the mistargeting of KOR1 and induce KOR1 accumulation in the tonoplast (TP). Yet, little is known about how retention and sorting of KOR1 are regulated in the PM-TGN cycle. Forward genetic screening for GFP-KOR1 mislocalizing phenotype resulted in several mutant lines with different localization patterns or signal intensity of GFP-KOR1. One of the identified mutants were disrupted at UDP-glucose:glycoprotein glucosyltransferase (UGGT) locus, which is essential for the protein quality control in the ER. Our finding suggests the mis/unfolded structure of KOR1 triggers the TP targeting.
Keyphrases
- quality control
- endoplasmic reticulum
- particulate matter
- genome wide
- type diabetes
- risk assessment
- heavy metals
- amino acid
- binding protein
- blood pressure
- adipose tissue
- dna methylation
- high resolution
- cancer therapy
- mass spectrometry
- endoplasmic reticulum stress
- polycyclic aromatic hydrocarbons
- wild type
- heat stress
- skeletal muscle
- functional connectivity
- cell wall
- genome wide association study
- breast cancer cells
- glycemic control