The function of the RNA-binding protein TEL1 in moss reveals ancient regulatory mechanisms of shoot development View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2012-03

AUTHORS

Julien Vivancos, Lara Spinner, Christelle Mazubert, Florence Charlot, Nicolas Paquet, Vincent Thareau, Michel Dron, Fabien Nogué, Céline Charon

ABSTRACT

The shoot represents the basic body plan in land plants. It consists of a repeated structure composed of stems and leaves. Whereas vascular plants generate a shoot in their diploid phase, non-vascular plants such as mosses form a shoot (called the gametophore) in their haploid generation. The evolution of regulatory mechanisms or genetic networks used in the development of these two kinds of shoots is unclear. TERMINAL EAR1-like genes have been involved in diploid shoot development in vascular plants. Here, we show that disruption of PpTEL1 from the moss Physcomitrella patens, causes reduced protonema growth and gametophore initiation, as well as defects in gametophore development. Leafy shoots formed on ΔTEL1 mutants exhibit shorter stems with more leaves per shoot, suggesting an accelerated leaf initiation (shortened plastochron), a phenotype shared with the Poaceae vascular plants TE1 and PLA2/LHD2 mutants. Moreover, the positive correlation between plastochron length and leaf size observed in ΔTEL1 mutants suggests a conserved compensatory mechanism correlating leaf growth and leaf initiation rate that would minimize overall changes in plant biomass. The RNA-binding protein encoded by PpTEL1 contains two N-terminus RNA-recognition motifs, and a third C-terminus non-canonical RRM, specific to TEL proteins. Removal of the PpTEL1 C-terminus (including this third RRM) or only 16-18 amino acids within it seriously impairs PpTEL1 function, suggesting a critical role for this third RRM. These results show a conserved function of the RNA-binding PpTEL1 protein in the regulation of shoot development, from early ancestors to vascular plants, that depends on the third TEL-specific RRM. More... »

PAGES

323-336

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s11103-011-9867-9

DOI

http://dx.doi.org/10.1007/s11103-011-9867-9

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1043106475

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/22170036


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