SHOOT MERISTEMLESS trafficking controls axillary meristem formation, meristem size and organ boundaries in Arabidopsis

• Published in: The Plant journal : for cell and molecular biology 2017-05, Vol.90 (3), p.435-446
• Main Authors: Balkunde, Rachappa, Kitagawa, Munenori, Xu, Xianfeng Morgan, Wang, Jing, Jackson, David
• Format: Article
• Language: English
• Subjects: Apical dominance; Arabidopsis; Arabidopsis - metabolism; Arabidopsis Proteins - metabolism; Autosomal dominant inheritance; axillary meristem; Biological Transport - genetics; Biological Transport - physiology; Botany; Boundaries; boundary; Corn; CUP SHAPED COTYLEDON; Dominance; Embryogenesis; Embryonic growth stage; Gene expression; Gene Expression Regulation, Developmental - genetics; Gene Expression Regulation, Developmental - physiology; Gene Expression Regulation, Plant - genetics; Gene Expression Regulation, Plant - physiology; Genes; Homeobox; Homology; Localization; Meristem - metabolism; Mobility; mRNA; Plant Shoots - metabolism; Plasmodesmata; Plasmodesmata - metabolism; Protein transport; Proteins; shoot apical meristem; SHOOT MERISTEMLESS; Stem cells; trafficking; Transcription; Zea mays
• ISSN: 0960-7412; 1365-313X
• DOI: 10.1111/tpj.13504

Summary The shoot stem cell niche, contained within the shoot apical meristem (SAM) is maintained in Arabidopsis by the homeodomain protein SHOOT MERISTEMLESS (STM). STM is a mobile protein that traffics cell‐to‐cell, presumably through plasmodesmata. In maize, the STM homolog KNOTTED1 shows clear differences between mRNA and protein localization domains in the SAM. However, the STM mRNA and protein localization domains are not obviously different in Arabidopsis, and the functional relevance of STM mobility is unknown. Using a non‐mobile version of STM (2xNLS‐YFP‐STM), we show that STM mobility is required to suppress axillary meristem formation during embryogenesis, to maintain meristem size, and to precisely specify organ boundaries throughout development. STM and organ boundary genes CUP SHAPED COTYLEDON1 (CUC1), CUC2 and CUC3 regulate each other during embryogenesis to establish the embryonic SAM and to specify cotyledon boundaries, and STM controls CUC expression post‐embryonically at organ boundary domains. We show that organ boundary specification by correct spatial expression of CUC genes requires STM mobility in the meristem. Our data suggest that STM mobility is critical for its normal function in shoot stem cell control. Significance Statement The maize KNOTTED1 protein acts non‐cell autonomously and trafficks cell‐to‐cell, presumably through plasmodesmata, but demonstrating a role for its trafficking (or of its Arabidopsis homolog SHOOT MERISTEMLESS) in the shoot stem cell niche has remained elusive. Here we use a non‐mobile STM protein to show that trafficking is important for both full meristem function and for boundary establishment and apical dominance.