A Molecular Framework for the Control of Adventitious Rooting by TIR1/AFB2-Aux/IAA-Dependent Auxin Signaling in Arabidopsis

0517176 - ÚEB 2020 RIV GB eng J - Článek v odborném periodiku
Lakehal, A. - Chaabouni, S. - Cavel, E. - Le Hir, R. - Ranjan, A. - Raneshan, Z. - Novák, Ondřej - Păcurar, D. I. - Perrone, I. - Jobert, F. - Gutierrez, L. - Bakò, L. - Bellini, C.
A Molecular Framework for the Control of Adventitious Rooting by TIR1/AFB2-Aux/IAA-Dependent Auxin Signaling in Arabidopsis.
Molecular Plant. Roč. 12, č. 11 (2019), s. 1499-1514. ISSN 1674-2052. E-ISSN 1752-9867
Grant CEP: GA MŠMT(CZ) EF16_019/0000827
Institucionální podpora: RVO:61389030
Klíčová slova: adventitious roots * Arabidopsis * AuxIAA * jasmonate * tir1/afb
Obor OECD: Biochemistry and molecular biology
Impakt faktor: 12.084, rok: 2019
Způsob publikování: Open access
http://dx.doi.org/10.1016/j.molp.2019.09.001

In Arabidopsis thaliana, canonical auxin-dependent gene regulation is mediated by 23 transcription factors from the AUXIN RESPONSE FACTOR (ARF) family that interact with auxin/indole acetic acid repressors (Aux/IAAs), which themselves form co-receptor complexes with one of six TRANSPORT INHIBITOR1/AUXIN-SIGNALLING F-BOX (TIR1/AFB) proteins. Different combinations of co-receptors drive specific sensing outputs, allowing auxin to control a myriad of processes. ARF6 and ARF8 are positive regulators of adventitious root initiation upstream of jasmonate, but the exact auxin co-receptor complexes controlling the transcriptional activity of these proteins has remained unknown. Here, using loss-of-function mutants we show that three Aux/IAA genes, IAA6, IAA9, and IAA17, act additively in the control of adventitious root (AR) initiation. These three IAA proteins interact with ARF6 and/or ARF8 and likely repress their activity in AR development. We show that TIR1 and AFB2 are positive regulators of AR formation and TIR1 plays a dual role in the control of jasmonic acid (JA) biosynthesis and conjugation, as several JA biosynthesis genes are up-regulated in the tir1-1 mutant. These results lead us to propose that in the presence of auxin, TIR1 and AFB2 form specific sensing complexes with IAA6, IAA9, and/or IAA17 to modulate JA homeostasis and control AR initiation.
Trvalý link: http://hdl.handle.net/11104/0302655