ArticlePlanta2023
The inhibition of maize (Zea mays L.) root stem cell regeneration by low oxygen is attenuated by Phytoglobin 1 (Pgb1) through changes in auxin and jasmonic acid.
Article in Planta, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- Duet between sugars and hormones: The molecular dialogue fine-tuning hypoxia acclimation in plants.Journal of integrative plant biology · 2026Review
- Discrete and cell-specific hypoxic responses in Arabidopsis roots resolved by single-nuclei transcriptomics.The New phytologist · 2026Article
- Preserving root stem cell functionality under low oxygen stress: the role of nitric oxide and phytoglobins.Planta · 2023Review
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Authors and funding
4 authors at 2 institutions in 2 countries.
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Abstract
MAIN
conclusionsOver-expression of Phytoglobin1 increases the viability of maize root stem cells to low oxygen stress through changes in auxin and jasmonic acid responses. Hypoxia inhibits maize (Zea mays L.) root growth by deteriorating the quiescent center (QC) stem cells of the root apical meristem. Over-expression of the Phytoglobin1 ZmPgb1.1 alleviates these effects through the retention of the auxin flow along the root profile required for the specification of the QC stem cells. To identify QC-specific hypoxia responses and determine whether ZmPgb1.1 exercises a direct role on QC stem cells, we performed a QC functionality test. This was done by estimating the ability of QCs to regenerate a root in vitro in a hypoxic environment. Hypoxia decreased the functionality of the QCs by depressing the expression of several genes participating in the synthesis and response of auxin. This was accompanied by a decrease in DR5 signal, a suppression of PLETHORA and WOX5, two markers of QC cell identity, and a reduction in expression of genes participating in JA synthesis and signaling. Over-expression of ZmPgb1.1 was sufficient to mitigate all these responses. Through pharmacological alterations of auxin and JA, it is demonstrated that both hormones are required for QC functionality under hypoxia, and that JA acts downstream of auxin during QC regeneration. A model is proposed whereby the ZmPgb1.1 maintenance of auxin synthesis in hypoxic QCs is determinant for the retention of their functionality, with JA supporting the regeneration of roots from the QCs.
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Registered trials
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