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Evolution of buffering in a genetic circuit controlling plant stem cell proliferation

2019; Nature Portfolio; Volume: 51; Issue: 5 Linguagem: Inglês

10.1038/s41588-019-0389-8

1546-1718

Daniel Rodríguez-Leal, Xu Cao, Choon‐Tak Kwon, Cara L. Soyars, Edgar Demesa-Arévalo, Jarrett Man, Lei Liu, Zachary H. Lemmon, Daniel S. Jones, Joyce Van Eck, David Jackson, Madelaine Bartlett, Zachary L. Nimchuk, Zachary B. Lippman,

Plant-Microbe Interactions and Immunity

Precise control of plant stem cell proliferation is necessary for the continuous and reproducible development of plant organs1,2. The peptide ligand CLAVATA3 (CLV3) and its receptor protein kinase CLAVATA1 (CLV1) maintain stem cell homeostasis within a deeply conserved negative feedback circuit1,2. In Arabidopsis, CLV1 paralogs also contribute to homeostasis, by compensating for the loss of CLV1 through transcriptional upregulation3. Here, we show that compensation4,5 operates in diverse lineages for both ligands and receptors, but while the core CLV signaling module is conserved, compensation mechanisms have diversified. Transcriptional compensation between ligand paralogs operates in tomato, facilitated by an ancient gene duplication that impacted the domestication of fruit size. In contrast, we found little evidence for transcriptional compensation between ligands in Arabidopsis and maize, and receptor compensation differs between tomato and Arabidopsis. Our findings show that compensation among ligand and receptor paralogs is critical for stem cell homeostasis, but that diverse genetic mechanisms buffer conserved developmental programs. A study of a stem cell receptor–ligand signaling module across tomato, maize and Arabidopsis identifies different genetic mechanisms of compensation that contribute to homeostasis.