Regulation of inflorescence architecture by intertissue layer ligand—receptor communication between endodermis and phloem
Multicellular organisms achieve final body shape and size by coordinating cell proliferation, expansion, and differentiation. Loss of function in the Arabidopsis ERECTA (ER) receptor-kinase gene confers characteristic compact inflorescence architecture, but its underlying signaling pathways remain u...
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Published in | Proceedings of the National Academy of Sciences - PNAS Vol. 109; no. 16; pp. 6337 - 6342 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
National Academy of Sciences
17.04.2012
National Acad Sciences |
Subjects | |
Online Access | Get full text |
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Summary: | Multicellular organisms achieve final body shape and size by coordinating cell proliferation, expansion, and differentiation. Loss of function in the Arabidopsis ERECTA (ER) receptor-kinase gene confers characteristic compact inflorescence architecture, but its underlying signaling pathways remain unknown. Here we report that the expression of ER in the phloem is sufficient to rescue compact er inflorescences. We further identified two EPIDERMAL PATTERNING FACTOR-LIKE (EPFL) secreted peptide genes, EPFL4 and EPFL6/CHALLAH (CHAL), as redundant, upstream components of ER-mediated inflorescence growth. The expression of EPFL4 or EPFL6 in the endodermis, a layer adjacent to phloem, is sufficient to rescue the er-like inflorescence of epfl4 epfl6 plants. EPFL4 and EPFL6 physically associate with ER in planta. Finally, transcriptome analysis of er and epfl4 epfl6 revealed a potential downstream component as well as a role for plant hormones in EPFL4/6- and ER-mediated inflorescence growth. Our results suggest that intercell layer communication between the endodermis and phloem mediated by peptide ligands and a receptor kinase coordinates proper inflorescence architecture in Arabidopsis. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Edited by Mark Estelle, University of California at San Diego, La Jolla, CA, and approved March 1, 2012 (received for review October 29, 2011) 1N.U. and J.S.L. contributed equally to this work. Author contributions: N.U., J.S.L., M.T., and K.U.T. designed research; N.U., J.S.L., H.-H.L., and K.U.T. performed research; N.U., J.S.L., R.K., T.K., and K.U.T. contributed new reagents/analytic tools; N.U., J.S.L., R.J.H., and K.U.T. analyzed data; and N.U., J.S.L., R.J.H., and K.U.T. wrote the paper. |
ISSN: | 0027-8424 1091-6490 |
DOI: | 10.1073/pnas.1117537109 |