These authors contributed equally to this work.
The tomato SlSHINE3 transcription factor regulates fruit cuticle formation and epidermal patterning
Article first published online: 3 DEC 2012
© 2012 The Authors. New Phytologist © 2012 New Phytologist Trust
Volume 197, Issue 2, pages 468–480, January 2013
How to Cite
Shi, J. X., Adato, A., Alkan, N., He, Y., Lashbrooke, J., Matas, A. J., Meir, S., Malitsky, S., Isaacson, T., Prusky, D., Leshkowitz, D., Schreiber, L., Granell, A. R., Widemann, E., Grausem, B., Pinot, F., Rose, J. K. C., Rogachev, I., Rothan, C. and Aharoni, A. (2013), The tomato SlSHINE3 transcription factor regulates fruit cuticle formation and epidermal patterning. New Phytologist, 197: 468–480. doi: 10.1111/nph.12032
- Issue published online: 18 DEC 2012
- Article first published online: 3 DEC 2012
- Manuscript Accepted: 4 OCT 2012
- Manuscript Received: 26 JUL 2012
- Israel Science Foundation
- European Research Council
- Agence Nationale de la Recherche. Grant Number: ANR-09-KBBE-006-001
- NSF Plant Genome Research Program. Grant Number: DBI-0606595
- United States-Israel Binational Agricultural Research and Development Fund. Grant Number: IS-4234-09
- CUAES-Hatch. Grant Number: NYC-18442
- epidermal cell patterning;
- Solanum lycopersicum ;
- surface architecture;
- transcriptional regulation;
- Fleshy tomato fruit typically lacks stomata; therefore, a proper cuticle is particularly vital for fruit development and interaction with the surroundings. Here, we characterized the tomato SlSHINE3 (SlSHN3) transcription factor to extend our limited knowledge regarding the regulation of cuticle formation in fleshy fruits.
- We created SlSHN3 overexpressing and silenced plants, and used them for detailed analysis of cuticular lipid compositions, phenotypic characterization, and the study on the mode of SlSHN3 action.
- Heterologous expression of SlSHN3 in Arabidopsis phenocopied overexpression of the Arabidopsis SHNs. Silencing of SlSHN3 results in profound morphological alterations of the fruit epidermis and significant reduction in cuticular lipids. We demonstrated that SlSHN3 activity is mediated by control of genes associated with cutin metabolism and epidermal cell patterning. As with SlSHN3 RNAi lines, mutation in the SlSHN3 target gene, SlCYP86A69, resulted in severe cutin deficiency and altered fruit surface architecture. In vitro activity assays demonstrated that SlCYP86A69 possesses NADPH-dependent ω-hydroxylation activity, particularly of C18:1 fatty acid to the 18-hydroxyoleic acid cutin monomer.
- This study provided insights into transcriptional mechanisms mediating fleshy fruit cuticle formation and highlighted the link between cutin metabolism and the process of fruit epidermal cell patterning.