MIXTA-Like Transcription Factors and WAX INDUCER1/SHINE1 Coordinately Regulate Cuticle Development inArabidopsisandTorenia fournieri   

Abstract

The waxy plant cuticle protects cells from dehydration, repels pathogen attack, and prevents organ fusion during development. The transcription factor WAX INDUCER1/SHINE1 (WIN1/SHN1) regulates the biosynthesis of waxy substances in Arabidopsis thaliana. Here, we show that the MIXTA-like MYB transcription factors MYB106 and MYB16, which regulate epidermal cell morphology, also regulate cuticle development coordinately with WIN1/SHN1 in Arabidopsis and Torenia fournieri. Expression of a MYB106 chimeric repressor fusion (35S:MYB106-SRDX) and knockout/down of MYB106 and MYB16 induced cuticle deficiencies characterized by organ adhesion and reduction of epicuticular wax crystals and cutin nanoridges. A similar organ fusion phenotype was produced by expression of a WIN1/SHN1 chimeric repressor. Conversely, the dominant active form of MYB106 (35S:MYB106-VP16) induced ectopic production of cutin nanoridges and increased expression of WIN1/ SHN1 and wax biosynthetic genes. Microarray experiments revealed that MYB106 and WIN1/SHN1 regulate similar sets of genes, predominantly those involved in wax and cutin biosynthesis. Furthermore, WIN1/SHN1 expression was induced by MYB106-VP16 and repressed by MYB106-SRDX. These results indicate that the regulatory cascade of MIXTA-like proteins and WIN1/SHN1 coordinately regulate cutin biosynthesis and wax accumulation. This study reveals an additional key aspect of MIXTA-like protein function and suggests a unique relationship between cuticle development and epidermal cell differentiation.

Analyses of Tomato Fruit Brightness Mutants Uncover Both Cutin-Deficient and Cutin-Abundant Mutants and a New Hypomorphic Allele of GDSL Lipase

“…However, the most striking result is that the dull fruit aspect of tomato cuticle mutants appears primarily due to different epidermal cell differentiation. The relationship between epidermal cell differentiation and cuticle development is now well established and genes controlling both cell morphogenesis and cuticle synthesis have been identified (Kurdyukov et al, 2006;Javelle et al, 2011;Oshima et al, 2013). More indirect effects may also arise from perturbations in fruit cell division and development that affect cuticle formation in tomato fruit (Czerednik et al, 2012).…”

“…Coordinated regulation of metabolic pathways controlling cuticle formation has been demonstrated for transcription factors of the SHINE/WAX-INDUCER family (Aharoni et al, 2004;Broun et al, 2004) and recently for MIXTA-like myeloblastosis (MYB) transcription factors (Oshima et al, 2013). Several of their downstream targets involved in cutin synthesis, modification, and assembly, as well as in cell wall formation and structure and in epidermal cell patterning (Shi et al, 2013), have been identified.…”

Enhanced cuticle accumulation by employing MIXTA-like transcription factors

“…Using these mutant lines, we showed that MYB106 and MYB16 are required for the formation of cuticle nanoridges in petals and stamens. Furthermore, we reported that MYB106 is sufficient for the ectopic production of nanoridges (Oshima et al 2013a). However, plants over-expressing MYB106 exhibit severe dwarfism and are not suitable for commercial production.…”

“…Additionally, the genes encoding these transporters are expressed in epidermal cells (Bird et al 2007;Luo et al 2007;Panikashvili et al 2007;Pighin et al 2004). The expression of ABCG12, CYP77A6, and CYP86A4 is suppressed in loss-of-function lines, but induced in gain-of-function lines involving the MYB106/NOECK MIXTA-like transcription factor (TF), which regulates cuticle production (Oshima et al 2013a).…”

“…We previously revealed that MYB106 and MYB16, which is the closest MYB106 paralog, regulate cuticle development in Arabidopsis thaliana and Torenia fournieri (Oshima et al 2013a;Oshima and Mitsuda 2013b). In vegetative organs, the null mutation of MYB106 does not lead to cuticular deficiencies except in trichomes.…”