Abstract
Hormone patterns tailor cell fate decisions during plant organ formation. Among them, auxins and cytokinins are critical phytohormones during early development. Nitric oxide (NO) modulates root architecture by the control of auxin spatial patterns. However, NO involvement during the coordination of shoot organogenesis remains unclear. Here, we explore the effect of NO during shoot development by using a phenotypic, cellular, and genetic analysis in Arabidopsis thaliana and get new insights into the characterization of NO-mediated leaf-related phenotypes. NO homeostasis mutants are impaired in several shoot architectural parameters, including phyllotactic patterns, inflorescence stem elongation, silique production, leaf number, and margin. Auxin distribution is a key feature for tissue differentiation and need to be controlled at different levels (i.e., synthesis, transport, and degradation mechanisms). The phenotypes resulting from the introduction of the cue1 mutation in the axr1 auxin resistant and pin1 backgrounds exacerbate the relationship between NO and auxins. Using the auxin reporter DR5:GUS, we observed an increase in auxin maxima under NO-deficient mutant backgrounds and NO scavenging, pointing to NO-ASSOCIATED 1 (NOA1) as the main player related to NO production in this process. Furthermore, polar auxin transport is mainly regulated by PIN-FORMED 1 (PIN1), which controls the flow along leaf margin and venations. Analysis of PIN1 protein levels shows that NO controls its accumulation during leaf development, impacting the auxin mediated mechanism of leaf building. With these findings, we also provide evidence for the NO opposite effects to determine root and shoot architecture, in terms of PIN1 accumulation under NO overproduction.
Highlights
Leaf initiation from the shoot apical meristem (SAM), and later development are controlled by networks composed by plant hormones and transcriptional factors, which determine organ form and size
In order to deepen on the nitric oxide (NO) and auxin crosstalk, we studied the weakened phenotypes resulting from the introduction of cue1 mutation in auxin resistant 1 background, and in pin1 mutant
Murray (Cardiff University, Cardiff, United Kingdom), nia1nia2noa1-2 mutant was a kind gift from Dr José León (IBMCP-CSIC, Valencia, Spain), and venosa and dov1 mutants were kindly provided by Dr José Luis Micol (UMH, Elche, Spain). axr1-3 mutant was generated by mutagenizing a Col-0 population with EMS (Lincoln et al, 1990), and it harbors a point mutation that changes a cysteine from the active site into an alanine, rendering the protein inactive
Summary
Leaf initiation from the shoot apical meristem (SAM), and later development are controlled by networks composed by plant hormones and transcriptional factors, which determine organ form and size. Specific points of auxin maxima are described previously to leaf initiation, involving changes in the polar localization of efflux carriers [i.e., PIN-FORMED (PIN1) proteins]. During the regulation of physiological and stress processes, the gasotransmitter nitric oxide (NO) usually interacts with plant hormones and other endogenous molecules, affecting their biosynthesis, catabolism, transport, perception, and signal transduction (reviewed in Freschi, 2013; Sanz et al, 2015). Knocking out phytoglobins (PGBs), which increase endogenous NO levels, inhibits auxin metabolism, resulting in a drastic modification of embryogenesis and root development (Elhiti et al, 2013)
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