Staff Publications

Staff Publications

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    'Staff publications' is the digital repository of Wageningen University & Research

    'Staff publications' contains references to publications authored by Wageningen University staff from 1976 onward.

    Publications authored by the staff of the Research Institutes are available from 1995 onwards.

    Full text documents are added when available. The database is updated daily and currently holds about 240,000 items, of which 72,000 in open access.

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Record number 495313
Title A bHLH-Based Feedback Loop Restricts Vascular Cell Proliferation in Plants
Author(s) Vera-Sirera, Francisco; Rybel, B.P.M. de; Urbez, Cristina; Kouklas, Evangelos; Pesquera, Marta; Alvarez-Mahecha, Juan Camilo; Minguet, Eugenio; Tuominen, Hanneke; Carbonell, Juan; Borst, J.W.; Weijers, D.; Blazquez, Miguel
Source Developmental cell 35 (2015)4. - ISSN 1534-5807 - p. 432 - 443.
DOI https://doi.org/10.1016/j.devcel.2015.10.022
Department(s) Biochemistry
EPS
Publication type Refereed Article in a scientific journal
Publication year 2015
Abstract Control of tissue dimensions in multicellular organisms requires the precise quantitative regulation of mitotic activity. In plants, where cells are immobile,
tissue size is achieved through control of both cell division orientation and mitotic rate. The bHLH transcription factor heterodimer formed by TARGET OF
MONOPTEROS5 (TMO5) and LONESOME HIGHWAY (LHW) is a central regulator of vascular widthincreasing divisions. An important unanswered question
is how its activity is limited to specify vascular tissue dimensions. Here we identify a regulatory network that restricts TMO5/LHW activity. We show
that thermospermine synthase ACAULIS5 antagonizes TMO5/LHW activity by promoting the accumulation of SAC51-LIKE (SACL) bHLH transcription
factors. SACL proteins heterodimerize with LHW—therefore likely competing with TMO5/LHW interactions—prevent activation ofTMO5/LHWtarget genes,
and suppress the over-proliferation caused by excess TMO5/LHWactivity. These findings connect two thusfar disparate pathways and provide a mechanistic
understanding of the quantitative control of vascular tissue growth.
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