Papillae formation on trichome cell walls requires the function of the mediator complex subunit Med25
Glassy Hair 1 (GLH1) gene that promotes papillae formation on trichome cell walls was identified as a subunit of the transcriptional mediator complex MED25. The MED25 gene is shown to be expressed in trichomes. The expression of the trichome development marker genes GLABRA2 (GL2) and Ethylene Receptor2 (ETR2) is not affected in the glh1 mutant. Presented data suggest that Arabidopsis MED25 mediator component is likely involved in the transcription of genes promoting papillae deposition in trichomes.
The plant cell wall plays an important role in communication, defense, organization and support. The importance of each of these functions varies by cell type. Specialized cells, such as Arabidopsis trichomes, exhibit distinct cell wall characteristics including papillae. To better understand the molecular processes important for papillae deposition on the cell wall surface, we identified the GLASSY HAIR 1 (GLH1) gene, which is necessary for papillae formation. We found that a splice-site mutation in the component of the transcriptional mediator complex MED25 gene is responsible for the near papillae-less phenotype of the glh1 mutant. The MED25 gene is expressed in trichomes. Reporters for trichome developmental marker genes GLABRA2 (GL2) and Ethylene Receptor2 (ETR2) were not affected in the glh1 mutant. Collectively, the presented results show that MED25 is necessary for papillae formation on the cell wall surface of leaf trichomes and suggest that the Arabidopsis MED25 mediator component is likely involved in the transcription of a subset of genes that promote papillae deposition in trichomes.
KeywordsCell wall Trichomes Papillae Mediator
The authors would like to thank Stephanie Seifert for her help with the genetic mapping of the GLH1 gene. Thanks are due to the Arabidopsis Biological Resource Center (http://abrc.osu.edu), from which we obtained T-DNA lines. We would like to acknowledge Dr. Pablo Cerdan for sending us the pPZP212 vector containing the MED25 regulatory and coding regions (Iñigo et al. 2012), and Dr. Sharon Regan at Queen’s University, Ontario Canada, for sending us ETR2pro::GUS lines (Plett et al. 2009). We also extend our appreciation to Dr. Martha Cook for her help with the SEM imaging and to Dr. Jun-Hyun Kim and Tony Ludwig for their help with the ICP analysis. This research was supported by Illinois State University (CF, BS, and VK) and by a Weigel Grant from the Beta Lambda chapter of Phi-Sigma Biological Society to CF.
CM, BS, MZ, KJ and VK designed and performed experiments. CM and VK have written the manuscript.
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