CYCLOIDEA paralogs function partially redundantly to specify dorsal flower development in Mimulus lewisii

Author:

Dunivant Taryn S.1,Singh Vibhuti1,Livingston Kaylee E.1,Ross Jack D.1,Hileman Lena C.1ORCID

Affiliation:

1. Department of Ecology and Evolutionary Biology University of Kansas 1200 Sunnyside Avenue Lawrence KS 66045 USA

Abstract

AbstractPremiseDuplicated genes (paralogs) are abundant in plant genomes, and their retention may influence the function of genetic programs and contribute to evolutionary novelty. How gene duplication affects genetic modules and what forces contribute to paralog retention are outstanding questions. The CYCLOIDEA(CYC)‐dependent flower symmetry program is a model for understanding the evolution of gene duplication, providing multiple examples of paralog partitioning and novelty. However, a novel CYC gene lineage duplication event near the origin of higher core Lamiales (HCL) has received little attention.MethodsTo understand the evolutionary fate of duplicated HCL CYC2 genes, we determined the effects on flower symmetry by suppressing MlCYC2A and MlCYC2B expression using RNA interference (RNAi). We determined the phenotypic effects on flower symmetry in single‐ and double‐silenced backgrounds and coupled our functional analyses with expression surveys of MlCYC2A, MlCYC2B, and a putative downstream RADIALIS (MlRAD5) ortholog.ResultsMlCYC2A and MlCYC2B jointly contribute to bilateral flower symmetry. MlCYC2B exhibits a clear dorsal flower identity function and may additionally function in carpel development. MlCYC2A functions in establishing dorsal petal shape. Further, our results suggest an MlCYC2A–MlCYC2B regulatory interaction, which may affect pathway homeostasis.ConclusionsOur results suggest that CYC paralogs specific to higher core Lamiales may be selectively retained for their joint contribution to bilateral flower symmetry, similar to the independently derived CYC paralogs in the Lamiales model for bilateral flower symmetry research, Antirrhinum majus (snapdragon).

Publisher

Wiley

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