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Shoot branching is a critical determinant of plant architecture and a key factor affecting crop yield. The shoot branching involves two main processes: axillary meristem formation and subsequent bud outgrowth. While considerable progress has been made in elucidating the genetic mechanisms underlying the latter process, our understanding of the former process remains limited. Rice FINE CULM1 (FC1), which is an ortholog of teosinte branched1 in maize (Zea mays) and BRANCHED1 / 2 in Arabidopsis (Arabidopsis thaliana), is known to act in the latter process by repressing bud outgrowth. In this study, we found that FC1 also plays a role in the former process, i.e. axillary meristem formation, in rice. This study was triggered by our unexpected observation that fc1 mutation suppresses the loss of axillary meristems in the loss-of-function mutant of the rice WUSCHEL gene TILLERS ABSENT1 (TAB1). In tab1 fc1 , unlike in tab1 , both stem cells and undifferentiated cells were maintained during axillary meristem formation, similar to the wild type. Morphological analysis showed that axillary meristem formation was accelerated in fc1 , compared to the wild type. Consistent with this, cell proliferation was more active in the region containing stem cells and undifferentiated cells during axillary meristem formation in fc1 than in the wild type. Taken altogether, these findings suggest that FC1 negatively regulates axillary meristem formation by mildly repressing cell proliferation during this process. [ABSTRACT FROM AUTHOR]

Lotus japonicus-ROOT HAIR LESS1-LIKE1 (LRL1) of Arabidopsis thaliana encodes a basic helix-loop-helix (bHLH) transcription factor (TF) involved in root hair development. Root hair development is regulated by an elaborate transcriptional network, in which GLABRA2 (GL2), a key negative regulator, directly represses bHLH TF genes, including LRL1 and ROOT HAIR DEFECTIVE6 (RHD6). Although RHD6 and its paralogous TFs have been shown to connect downstream to genes involved in cell morphological events such as endomembrane and cell wall modification, the network downstream of LRL1 remains elusive. We found that a mutation of LRL1 causes a short-root-hair phenotype and that this phenotype can be partially rescued by a transgene encoding a glucocorticoid receptor (GR) domain-fused LRL1, LRL1-GR, in the presence of glucocorticoids. Using this conditional rescue system, we identified 46 genes that are activated downstream of LRL1. Among these, cell wall-related genes were significantly enriched and many of them were found to be immediately downstream of LRL1 without de novo protein synthesis in between. We further analyzed three representative genes, PROLINE-RICH PROTEIN1 (PRP1), PRP3, and XYLOGLUCAN ENDOTRANSGLUCOSYLASE/HYDOLASE12 (XTH12). Reporter gene analyses showed that these genes are specifically transcribed in root hair cells including those in the root-hypocotyl junction, and that their proteins were localized to the cell wall of elongating root hairs, root hair bulges, and root hair bulge-expecting loci. A T-DNA insertion mutant of PRP3 showed a moderate short-root-hair phenotype. Based on these results, LRL1 is likely to promote root hair development throughout the morphogenetic process by activating cell wall-related genes., (© The Author(s) 2025. Published by Oxford University Press on behalf of Japanese Society of Plant Physiologists. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site–for further information please contact journals.permissions@oup.com.)

In Arabidopsis, root hairs are formed only from a set of epidermal cells named trichoblasts or hair-forming cells. Previous studies showed CAPRICE (CPC) promotes differentiation of hair-forming cells by controlling a negative regulator, GLABRA2 (GL2), which is preferentially expressed in hairless cells. Here, we show that CPC is also predominantly expressed in the hairless cells, but not in the neighboring hair-forming cells, and that CPC protein moves to the hair-forming cells and represses the GL2 expression. We also show that the N terminus of bHLH protein interacts with CPC and is responsible for the GL2 expression. We propose a model in which CPC plays a key role in the fate-determination of hair-forming cells.