STM sustains stem cell function in the Arabidopsis shoot apical meristem and controls KNOX gene expression independently of the transcriptional repressor AS1

Scofield, Simon ORCID: https://orcid.org/0000-0001-5466-314X, Dewitte, Walter ORCID: https://orcid.org/0000-0002-0606-1686 and Murray, James Augustus Henry ORCID: https://orcid.org/0000-0002-2282-3839 2014. STM sustains stem cell function in the Arabidopsis shoot apical meristem and controls KNOX gene expression independently of the transcriptional repressor AS1. Plant Signaling and Behavior 9 (6) , e28934. 10.4161/psb.28934

Preview

PDF - Published Version Available under License Creative Commons Attribution. Download (853kB) | Preview

Abstract

The Arabidopsis KNOX gene SHOOT MERISTEMLESS (STM) is required for both the development and the sustained function of the shoot apical meristem (SAM) and can induce de novo meristem formation when expressed ectopically. STM acts through induction of cytokinin (CK) synthesis to inhibit cellular differentiation and additionally functions to organize undifferentiated cells into a self-sustaining meristem. STM has been shown to positively regulate the related KNOX genes KNAT1/BP and KNAT2, and it has been proposed that this is mediated through repression of the ARP-type transcriptional repressor ASYMMETRIC LEAVES1 (AS1). Here we investigate the role of STM in SAM organization, stem cell maintenance and the regulation of KNOX gene expression. We show that culture of stm mutant explants in high CK conditions does not restore proper sustained shoot growth, supporting the idea of STM having CK-independent roles in meristem function. Furthermore, we show that STM is required for continued stem cell function in the SAM by sustaining expression of the stem cell-promoting factor WUS and preventing cells of the meristem organizing center from adopting lateral organ-specific fates. We also demonstrate that transcriptional activation of class-1 KNOX genes by STM is independent of AS1, since AS1 transcript levels are not reduced in response to STM and STM is able to transactivate expression of both KNAT1/BP and KNAT2 in the as1 mutant background.

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Biosciences
Subjects:	Q Science > Q Science (General)
Publisher:	Landes Bioscience
ISSN:	1559-2316
Date of First Compliant Deposit:	30 March 2016
Date of Acceptance:	16 April 2014
Last Modified:	08 May 2023 21:43
URI:	https://orca.cardiff.ac.uk/id/eprint/60134

Citation Data

Cited 25 times in Scopus. View in Scopus. Powered By Scopus® Data

Actions (repository staff only)

Edit Item