Auxin and LANCEOLATE affect leaf shape in tomato via different developmental processes

Abstract

Elaboration of a complex leaves depends on the morphogenetic activity of a specific tissue at the leaf margin termed marginal-blastozon (MB). In tomato (Solanum lycopersicym), prolonged activity of the MB leads to the development of compound leaves. The activity of the MB is restricted by the TCP transcription factor LANCEOLATE (LA). Plants harboring the dominant LA mutant allele La-2 have simple leaves with a uniform blade. Conversely, leaves of pFIL > > miR319 are compound and grow indeterminately in their margins due to leaf overexpression of miR319, a negative regulator of LA and additional miR319-sensitive genes. We have recently shown that the auxin-response sensor DR5::VENUS marks and precedes leaflet initiation events in the MB. Mutations in ENTIRE (E), an auxin signal inhibitor from the Aux/IAA family, lead to the expansion of the DR5::VENUS signal to throughout the leaf-primordia margin, and to a simplified leaf phenotype. Here, we examined the interaction between auxin, E, and LA in tomato leaf development. In La-2 leaf primordia, the auxin signal is very weak and is diffused to throughout the leaf margin, suggesting that auxin acts within the developmental-context of MB activity, which is controlled by LA. e La-2 double mutants showed an enhanced simple leaf phenotype and e pFIL > > miR319 leaves initiated less leaflets than wild-type, but their margins showed continuous growth. These results suggest that E and auxin affect leaflet initiation within the context of the extended MB activity, but their influence on the extent of indeterminate growth of the leaf is minor.

Keywords: :

• Auxin
• CIN-TCP
• LANCEOLATE
• SlIAA9/ENTIRE
• Tomato
• compound leaf
• leaf development

Disclosure of Potential Conflicts of Interest

No potential conflicts of interest were disclosed.

Acknowledgments

This work was supported by grants from BARD (no. IS 04140–08C) and the Israeli Ministry of Agriculture (no. 837–0055–09) to NO. HB is funded in part by a Kaye Einstein Scholarship.