Endopolyploidization and flowering time are antagonistically regulated by checkpoint component MAD1 and immunity modulator MOS1

Zhilong Bao, Ning Zhang and Jian Hua ()
Additional contact information
Zhilong Bao: Cornell University
Ning Zhang: Cornell University
Jian Hua: Cornell University

Nature Communications, 2014, vol. 5, issue 1, 1-10

Abstract: Abstract The spindle assembly checkpoint complex (SAC) is essential for quality control during mitosis in yeast and animals. However, its function in plants is not well understood. Here we show that MAD1, an Arabidopsis SAC component, is involved in endopolyploidization and flowering time via genetic interaction with MOS1, a negative regulator of plant immunity. MOS1 is found to interact with MAD2, another SAC component, and promote flowering and inhibit endopolyploidization, but this function is antagonized by MAD1. Furthermore, MAD1 and MOS1 both interact with SUF4, a transcription factor regulating the expression of the flowering time gene FLC. These findings reveal MOS1, MAD1 and SUF4 as regulators of endopolyploidization and flowering time and suggest an involvement of cell cycle control in the timing of reproductive transition.

Date: 2014
References: Add references at CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/ncomms6628 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms6628

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/ncomms6628

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().