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. 2017 May;90(3):435-446.
doi: 10.1111/tpj.13504. Epub 2017 Mar 22.

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

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

Rachappa Balkunde et al. Plant J. 2017 May.
Free article

Erratum in

  • Correction.
    [No authors listed] [No authors listed] Plant J. 2017 Jun;90(6):1213. doi: 10.1111/tpj.13587. Plant J. 2017. PMID: 28585413 No abstract available.

Abstract

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.

Keywords: CUP SHAPED COTYLEDON; SHOOT MERISTEMLESS; axillary meristem; boundary; plasmodesmata; shoot apical meristem; trafficking.

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