PETAL LOSS, a trihelix transcription factor that represses growth in Arabidopsis thaliana, binds the energy-sensing SnRK1 kinase AKIN10

© The Author 2015. Published by Oxford University Press on behalf of the Society for Experimental Biology.

Bibliographische Detailangaben
Veröffentlicht in:Journal of experimental botany. - 1985. - 66(2015), 9 vom: 21. Mai, Seite 2475-85
1. Verfasser: O'Brien, Martin (VerfasserIn)
Weitere Verfasser: Kaplan-Levy, Ruth N, Quon, Tezz, Sappl, Pia G, Smyth, David R
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2015
Zugriff auf das übergeordnete Werk:Journal of experimental botany
Schlagworte:Journal Article Research Support, Non-U.S. Gov't AKIN10 Arabidopsis Golgi PETAL LOSS SnRK1 transcription factor trihelix. Arabidopsis Proteins mehr... PTL protein, Arabidopsis Transcription Factors Protein Serine-Threonine Kinases EC 2.7.11.1 SnRK1 protein, Arabidopsis
Beschreibung
Zusammenfassung:© The Author 2015. Published by Oxford University Press on behalf of the Society for Experimental Biology.
Organogenesis in plants involves differential growth. Rapidly growing primordia are distinguished from the meristem and each other by slower growing boundaries. PETAL LOSS (PTL) is a trihelix transcription factor of Arabidopsis that represses growth in boundaries between newly arising sepals. To identify partners involved in this growth limitation, a young inflorescence cDNA library was screened by yeast two-hybrid technology with PTL as bait. The most frequent prey identified was AKIN10, the catalytic α-subunit of the Snf1-related kinase1 (SnRK1). Interaction was mapped to the C-terminal (non-kinase) half of AKIN10 and the N-terminal portion of PTL. Binding of PTL was specific to AKIN10 as there was little binding to the related AKIN11. The interaction was confirmed by co-immunoprecipitation in vitro. Fluorescently tagged products of 35S:YFP-AKIN10 and 35S:CFP-PTL also interacted when transiently expressed together in leaf cells of Nicotiana benthamiana. In this case, most of the cytoplasmic AKIN10 was preferentially moved to the nucleus where PTL accumulated, possibly because a nuclear export sequence in AKIN10 was now masked. During these experiments, we observed that AKIN10 could variably accumulate in the Golgi, shown by its co-localization with a tagged Golgi marker and through its dispersal by brefeldin A. Tests of phosphorylation of PTL by AKIN10 gave negative results. The functional significance of the PTL-AKIN10 interaction remains open, although a testable hypothesis is that AKIN10 senses lower energy levels in inter-sepal zones and, in association with PTL, promotes reduced cell division
Beschreibung:Date Completed 09.02.2016
Date Revised 03.12.2021
published: Print-Electronic
Citation Status MEDLINE
ISSN:1460-2431
DOI:10.1093/jxb/erv032