ArticlePlanta2023
The Arabidopsis Phytoglobin 2 mediates phytochrome B (phyB) light signaling responses during somatic embryogenesis.
Article in Planta, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Establishment of a High-Frequency Plant Regeneration Protocol for the MultipurposePlants (Basel, Switzerland) · 2026Article
- MONOPTEROS isoform MP11ir plays a role during somatic embryogenesis in Arabidopsis thaliana.Plant physiology · 2025Article
- Transcriptional Dynamics Underlying Somatic Embryogenesis inPlants (Basel, Switzerland) · 2025Article
- Article
- How does light regulate plant regeneration?Frontiers in plant science · 2024Review
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Authors and funding
5 authors at 2 institutions in 2 countries.
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Abstract
MAIN
conclusionsDuring the light induction of somatic embryogenesis, phyB-Pfr suppresses Phytoglobin 2, known to elevate nitric oxide (NO). NO depresses Phytochrome Interacting Factor 4 (PIF4) relieving its inhibition on embryogenesis through auxin. An obligatory step of many in vitro embryogenic systems is the somatic-embryogenic transition culminating with the formation of the embryogenic tissue. In Arabidopsis, this transition requires light and is facilitated by high levels of nitric oxide (NO) generated by either suppression of the NO scavenger Phytoglobin 2 (Pgb2), or its removal from the nucleus. Using a previously characterized induction system regulating the cellular localization of Pgb2, we demonstrated the interplay between phytochrome B (phyB) and Pgb2 during the formation of embryogenic tissue. The deactivation of phyB in the dark coincides with the induction of Pgb2 known to reduce the level of NO; consequently, embryogenesis is inhibited. Under light conditions, the active form of phyB depresses the levels of Pgb2 transcripts, thus expecting an increase in cellular NO. Induction of Pgb2 increases Phytochrome Interacting Factor 4 (PIF4) suggesting that high levels of NO repress PIF4. The PIF4 inhibition is sufficient to induce several auxin biosynthetic (CYP79B2, AMI1, and YUCCA 1, 2, and 6) and response (ARF5, 8, and 16) genes, conducive to the formation of the embryonic tissue and production of somatic embryos. Auxin responses mediated by ARF10 and 17 appear to be regulated by Pgb2, possibly through NO, in a PIF4-independent fashion. Overall, this work provides a new and preliminary model integrating Pgb2 (and NO) with phyB in the light regulation of in vitro embryogenesis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.