Rice qGL3/OsPPKL1 Functions with the GSK3/SHAGGY-Like Kinase OsGSK3 to Modulate Brassinosteroid Signaling

Rice qGL3 negatively regulates brassinosteroid signaling by regulating the phosphorylation level and stability of OsGSK3, which modulates OsBZR1 phosphorylation status and subcellular distribution. Brassinosteroids (BRs) are steroid hormones that play essential roles in plant growth and development. We previously cloned qGL3, a major quantitative trait locus regulating grain length in rice (Oryza sativa). The O. sativa japonica var N411 has extra-large grains compared with the O. sativa indica var 9311, and the recessive qgl3 allele from N411 contributes positively to grain length. qGL3 encodes a putative protein phosphatase with Kelch-like repeat domains, an ortholog of Arabidopsis (Arabidopsis thaliana) brassinosteroid-insensitive1 SUPPRESSOR1 (BSU1). BSU1 positively regulates BR signaling, while overexpression of qGL3 induced BR loss-of-function phenotypes. Both qGL3N411 and qGL39311 physically interact with the rice glycogen synthase kinase 3 (GSK3)/SHAGGY-like kinase 3 (OsGSK3), an ortholog of Arabidopsis BR INSENSITIVE2 (BIN2). qGL39311 dephosphorylates OsGSK3, but qGL3N411 lacks this activity. Knocking out OsGSK3 enhances BR signaling and induces nuclear localization of O. sativa BRASSINAZOLE RESISTANT1 (OsBZR1). Unlike the dephosphorylation of BIN2 (which leads to protein degradation) in Arabidopsis, qGL3 dephosphorylates and stabilizes OsGSK3 in rice. These results demonstrate that qGL3 suppresses BR signaling by regulating the phosphorylation and stability of OsGSK3, which modulates OsBZR1 phosphorylation and subcellular distribution. Our study clarifies the role of qGL3 in the regulation of grain length and provides insight into BR signaling, including the differences between rice and Arabidopsis.

• Publication year

  2019

• Venue

  The Plant Cell

• Publication date

  2019-03-28

• Fields of study

  Biology, Medicine, Environmental Science

• Identifiers
  DOI 10.1105/tpc.18.00836PMID 30923230PMCID PMC6533024
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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