Abstract:Phosphate (Pi) is pivotal for plant growth and development. Pi deficiency triggers local and systemically regulated adaptive responses in Arabidopsis thaliana. Inhibition of primary root growth (PRG) and retarded development of lateral roots (LRs) are typical local Pi deficiency-mediated responses of the root system. Expression of Pi starvation-responsive (PSR) genes is regulated systemically. Here, we report the differential influence of iron (Fe) availability on local and systemic sensing of Pi by Arabidopsi… Show more
“…The Mediator (MED) complex is a multi-subunit complex that acts as a bridge between promoter-bound transcription factors and the RNA polymerase II transcription initiation complex to control gene expression. In plants, MED subunits participate in several developmental processes, hormonal signaling pathways, and biotic and abiotic stress tolerance (Manners and Kazan, 2009;Gillmor et al, 2010Gillmor et al, , 2014Ito et al, 2011;Xu and Li, 2011;C ßevik et al, 2012;Rai et al, 2014;Yang et al, 2014;Zhang et al, 2014;Raya-Gonz alez et al, 2014. However, how MED subunits could be interacting to determine the MED functioning per se on plant development remains largely unknown.…”
Summary
The Mediator (MED) complex plays a key role in the recruitment and assembly of the transcription machinery for the control of gene expression. Here, we report on the role of MEDIATOR18 (MED18) subunit in root development, auxin signaling and meristem cell viability in Arabidopsis thaliana seedlings. Loss‐of‐function mutations in MED18 reduce primary root growth, but increase lateral root formation and root hair development. This phenotype correlates with alterations in cell division and elongation likely caused by an increased auxin response and transport at the root tip, as evidenced by DR5:GFP, pPIN1::PIN1‐GFP, pPIN2::PIN2‐GFP and pPIN3::PIN3‐GFP auxin‐related gene expression. Noteworthy, med18 seedlings manifest cell death in the root meristem, which exacerbates with age and/or exposition to DNA‐damaging agents, and display high expression of the cell regeneration factor ERF115. Cell death in the root tip was reduced in med18 seedlings grown in darkness, but remained when only the shoot was exposed to light, suggesting that MED18 acts to protect root meristem cells from local cell death, and/or in response to root‐acting signal(s) emitted by the shoot in response to light stimuli. These data point to MED18 as an important component for auxin‐regulated root development, cell death and cell regeneration in root meristems.
“…The Mediator (MED) complex is a multi-subunit complex that acts as a bridge between promoter-bound transcription factors and the RNA polymerase II transcription initiation complex to control gene expression. In plants, MED subunits participate in several developmental processes, hormonal signaling pathways, and biotic and abiotic stress tolerance (Manners and Kazan, 2009;Gillmor et al, 2010Gillmor et al, , 2014Ito et al, 2011;Xu and Li, 2011;C ßevik et al, 2012;Rai et al, 2014;Yang et al, 2014;Zhang et al, 2014;Raya-Gonz alez et al, 2014. However, how MED subunits could be interacting to determine the MED functioning per se on plant development remains largely unknown.…”
Summary
The Mediator (MED) complex plays a key role in the recruitment and assembly of the transcription machinery for the control of gene expression. Here, we report on the role of MEDIATOR18 (MED18) subunit in root development, auxin signaling and meristem cell viability in Arabidopsis thaliana seedlings. Loss‐of‐function mutations in MED18 reduce primary root growth, but increase lateral root formation and root hair development. This phenotype correlates with alterations in cell division and elongation likely caused by an increased auxin response and transport at the root tip, as evidenced by DR5:GFP, pPIN1::PIN1‐GFP, pPIN2::PIN2‐GFP and pPIN3::PIN3‐GFP auxin‐related gene expression. Noteworthy, med18 seedlings manifest cell death in the root meristem, which exacerbates with age and/or exposition to DNA‐damaging agents, and display high expression of the cell regeneration factor ERF115. Cell death in the root tip was reduced in med18 seedlings grown in darkness, but remained when only the shoot was exposed to light, suggesting that MED18 acts to protect root meristem cells from local cell death, and/or in response to root‐acting signal(s) emitted by the shoot in response to light stimuli. These data point to MED18 as an important component for auxin‐regulated root development, cell death and cell regeneration in root meristems.
“…Therefore, it would be interesting to study the conservation and diversification of phytohormone mediated regulation of miR166/165, its target HD-ZIP IIIs across the plant species. Since both nutrient availability and phytohormones are known to regulate both miRNA expression and root development, it raises the possibility of regulation of these miRNAs through nutrient-phytohormone crosstalk, which remains an interesting area to be addressed 1, 41 .Figure 7A hypothetical model showing complex crosstalk among phytohormones, miR166/165, HD-ZIP IIIs and KAN genes regulating root growth. miR166/165 and HD-ZIP IIIs mediated root growth and development is regulated by various hormones such as IAA (red lines), GA (green lines), CK (grey lines), ABA (purple lines), JA (blue lines) and SA (orange lines) through transcriptional regulation of miR166/165, HD-ZIP IIIs and KAN genes.…”
Both phytohormones and non-coding microRNAs (miRNAs) play important role in root development in Arabidopsis thaliana. Mature miR166/165 s, which are derived from precursor transcripts of concerned genes, regulate developmental processes, including leaf and root patterning, by targeting Class III HOMEODOMAIN LEUCINE-ZIPPER (HD-ZIP III) transcription factors (TFs). However, their regulation through hormones remained poorly understood. Here, we show that several phytohormones dynamically regulate the spatio-temporal expression pattern of miR166/165 and target HD-ZIP IIIs in developing roots. Hormone signaling pathway mutants show differential expression pattern of miR166/165, providing further genetic evidence for multilayered regulation of these genes through phytohormones. We further show that a crosstalk of at least six different phytohormones regulate the miR166/165, their target HD-ZIP IIIs, and KANADI (KANs). Our results suggest that HD-ZIP IIIs mediated root development is modulated both transcriptionally through phytohormones and KANs, and post-transcriptionally by miR166/165 that in turn are also regulated by the phytohormonal crosstalk.
“…According to this view, ethylene, besides P and Fe deficiency responses, is also implicated in the induction of responses to K deficiency [138], to S deficiency [139,140], and to other deficiencies ( [3] and references therein). Recently, Rai et al [141] demonstrated the potential roles of auxin and Zinc (Zn) in mediating local Pi deficiency responses of the root system during growth under different Fe regimes, supporting the existence of crosstalk between Pi, Fe and Zn for maintaining Pi homeostasis.…”
Section: Crosstalk Among Fe and P Deficienciesmentioning
This review deals with two essential plant mineral nutrients, iron (Fe) and phosphorus (P); the acquisition of both has important environmental and economic implications. Both elements are abundant in soils but are scarcely available to plants. To prevent deficiency, dicot plants develop physiological and morphological responses in their roots to specifically acquire Fe or P. Hormones and signalling substances, like ethylene, auxin and nitric oxide (NO), are involved in the activation of nutrient-deficiency responses. The existence of common inducers suggests that they must act in conjunction with nutrient-specific signals in order to develop nutrient-specific deficiency responses. There is evidence suggesting that P-or Fe-related phloem signals could interact with ethylene and NO to confer specificity to the responses to Fe-or P-deficiency, avoiding their induction when ethylene and NO increase due to other nutrient deficiency or stress. The mechanisms responsible for such interaction are not clearly determined, and thus, the regulatory networks that allow or prevent cross talk between P and Fe deficiency responses remain obscure. Here, fragmented information is drawn together to provide a clearer overview of the mechanisms and molecular players involved in the regulation of the responses to Fe or P deficiency and their interactions.
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