Nitrate-induced CLE35 signaling peptides inhibit nodulation through the SUNN receptor and miR2111 repression.
Journal
Plant physiology
ISSN: 1532-2548
Titre abrégé: Plant Physiol
Pays: United States
ID NLM: 0401224
Informations de publication
Date de publication:
02 04 2021
02 04 2021
Historique:
received:
02
11
2020
accepted:
09
12
2020
pubmed:
2
4
2021
medline:
6
8
2021
entrez:
1
4
2021
Statut:
ppublish
Résumé
Legume plants form nitrogen (N)-fixing symbiotic nodules when mineral N is limiting in soils. As N fixation is energetically costly compared to mineral N acquisition, these N sources, and in particular nitrate, inhibit nodule formation and N fixation. Here, in the model legume Medicago truncatula, we characterized a CLAVATA3-like (CLE) signaling peptide, MtCLE35, the expression of which is upregulated locally by high-N environments and relies on the Nodule Inception-Like Protein (NLP) MtNLP1. MtCLE35 inhibits nodule formation by affecting rhizobial infections, depending on the Super Numeric Nodules (MtSUNN) receptor. In addition, high N or the ectopic expression of MtCLE35 represses the expression and accumulation of the miR2111 shoot-to-root systemic effector, thus inhibiting its positive effect on nodulation. Conversely, ectopic expression of miR2111 or downregulation of MtCLE35 by RNA interference increased miR2111 accumulation independently of the N environment, and thus partially bypasses the nodulation inhibitory action of nitrate. Overall, these results demonstrate that the MtNLP1-dependent, N-induced MtCLE35 signaling peptide acts through the MtSUNN receptor and the miR2111 systemic effector to inhibit nodulation.
Identifiants
pubmed: 33793938
pii: 6066196
doi: 10.1093/plphys/kiaa094
pmc: PMC8133669
doi:
Substances chimiques
MicroRNAs
0
Nitrates
0
Plant Proteins
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1216-1228Informations de copyright
© American Society of Plant Biologists 2021. All rights reserved. For permissions, please email: journals.permissions@oup.com.
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