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Updated: Jan 10, 2026

A Method for Characterizing Embryogenesis in Arabidopsis
Published on: August 4, 2017
MONOPTEROS isoform MP11ir plays a role during somatic embryogenesis in Arabidopsis thaliana
Barbara Wójcikowska1,2, Samia Belaidi1,3, Victoria Mironova4
1Hormonal Crosstalk in Plant Development, Mendel Centre for Plant Genomics and Proteomics, CEITEC MU - Central European Institute of Technology, Masaryk University, Brno 625 00, Czech Republic.
None:
Auxin is crucial for plant morphogenesis, including embryo development. Exogenous auxin application is necessary for inducing embryogenic responses in in vitro cultured explants of Arabidopsis (Arabidopsis thaliana) and other plants. Thus, components of auxin transport, signaling, and metabolism are key to somatic embryogenesis. AUXIN RESPONSE FACTOR (ARF) transcription factors bind to auxin response elements to control auxin-responsive gene expression and are often repressed by AUXIN/INDOLE-3-ACETIC ACIDs (Aux/IAAs). MONOPTEROS (MP)/ARF5 is especially important in the embryogenic transition, being highly expressed during somatic embryogenesis; its mutant cannot develop somatic embryos. The MP11ir transcript, an alternatively spliced variant of MP, produces a truncated protein missing the Phox and Bem1p (PB1) domain, crucial for ARF-Aux/IAA dimerization. This renders MP11ir insensitive to Aux/IAA repression, suggesting auxin-independent regulation. High levels of MP11ir transcript are observed during auxin- and trichostatin-A-dependent induction of somatic embryogenesis. Both MP and MP11ir are essential for embryo regeneration in the mpS319 mutant. However, overexpression of a truncated MP protein (ΔARF5) lacking the PB1 domain inhibits somatic embryogenesis, resulting in callus instead of somatic embryos. Overexpression of ΔARF5, lack of MP protein (mp mutant), or interference with MP action by the auxin-resistant BODENLOS (BDL) protein affects the expression of auxin biosynthesis genes. Our results suggest that these auxin-related genes might be targets of MP11ir and/or MP. Consequently, any adjustment to MP activity alters auxin homeostasis and endogenous auxin levels, hindering embryogenic transition.
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