scholarly journals Fine control of aerenchyma and lateral root development through AUX/IAA- and ARF-dependent auxin signaling

2019 ◽  
Vol 116 (41) ◽  
pp. 20770-20775 ◽  
Author(s):  
Takaki Yamauchi ◽  
Akihiro Tanaka ◽  
Hiroki Inahashi ◽  
Naoko K. Nishizawa ◽  
Nobuhiro Tsutsumi ◽  
...  
Keyword(s):  
Root Development ◽  
Molecular Mechanisms ◽  
Auxin Transport ◽  
Lateral Roots ◽  
Cortical Cell ◽  
Dominant Negative ◽  
Dominant Negative Effect ◽  
Auxin Signaling ◽  
Transport Inhibitor ◽  
Auxin Transport Inhibitor

Lateral roots (LRs) are derived from a parental root and contribute to water and nutrient uptake from the soil. Auxin/indole-3-acetic acid protein (AUX/IAA; IAA) and auxin response factor (ARF)-mediated signaling are essential for LR formation. Lysigenous aerenchyma, a gas space created by cortical cell death, aids internal oxygen transport within plants. Rice (Oryza sativa) forms lysigenous aerenchyma constitutively under aerobic conditions and increases its formation under oxygen-deficient conditions; however, the molecular mechanisms regulating constitutive aerenchyma (CA) formation remain unclear. LR number is reduced by the dominant-negative effect of a mutated AUX/IAA protein in the iaa13 mutant. We found that CA formation is also reduced in iaa13. We have identified ARF19 as an interactor of IAA13 and identified a lateral organ boundary domain (LBD)-containing protein (LBD1-8) as a target of ARF19. IAA13, ARF19, and LBD1-8 were highly expressed in the cortex and LR primordia, suggesting that these genes function in the initiation of CA and LR formation. Restoration of LBD1-8 expression recovered aerenchyma formation and partly recovered LR formation in the iaa13 background, in which LBD1-8 expression was reduced. An auxin transport inhibitor suppressed CA and LR formation, and a natural auxin stimulated CA formation in the presence of the auxin transport inhibitor. Our findings suggest that CA and LR formation are both regulated through AUX/IAA- and ARF-dependent auxin signaling. The initiation of CA formation lagged that of LR formation, which indicates that the formation of CA and LR are regulated differently by auxin signaling during root development in rice.

Lateral root formation and nutrients: nitrogen in the spotlight

2021 ◽  
Author(s):  
Pierre-Mathieu Pélissier ◽  
Hans Motte ◽  
Tom Beeckman
Keyword(s):  
Signaling Pathways ◽  
Root System ◽  
Root Development ◽  
Lateral Root ◽  
Molecular Mechanisms ◽  
Root Formation ◽  
Lateral Roots ◽  
Nutrient Use Efficiency ◽  
Lateral Root Formation ◽  
Lateral Root Development

Abstract Lateral roots are important to forage for nutrients due to their ability to increase the uptake area of a root system. Hence, it comes as no surprise that lateral root formation is affected by nutrients or nutrient starvation, and as such contributes to the root system plasticity. Understanding the molecular mechanisms regulating root adaptation dynamics towards nutrient availability is useful to optimize plant nutrient use efficiency. There is at present a profound, though still evolving, knowledge on lateral root pathways. Here, we aimed to review the intersection with nutrient signaling pathways to give an update on the regulation of lateral root development by nutrients, with a particular focus on nitrogen. Remarkably, it is for most nutrients not clear how lateral root formation is controlled. Only for nitrogen, one of the most dominant nutrients in the control of lateral root formation, the crosstalk with multiple key signals determining lateral root development is clearly shown. In this update, we first present a general overview of the current knowledge of how nutrients affect lateral root formation, followed by a deeper discussion on how nitrogen signaling pathways act on different lateral root-mediating mechanisms for which multiple recent studies yield insights.

Abstract 080: Eya4 Induces Hypertrophy Via Regulation Of p27kip1

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Tatjana Williams ◽  
Moritz Hundertmark ◽  
Peter Nordbeck ◽  
Sabine Voll ◽  
Melanie Muehlfelder ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Cardiac Hypertrophy ◽  
Molecular Mechanisms ◽  
Pressure Overload ◽  
Dominant Negative ◽  
Heart Weight ◽  
Dominant Negative Effect ◽  
Mutant Form ◽  
Cardiac Phenotype ◽  
Truncating Mutation

Introduction: E193, a truncating mutation in the transcription cofactor Eyes absent 4 (Eya4) causes hearing impairment followed by heart failure. Here we identified the Eya4 dependent molecular mechanisms leading to the cardiac phenotype in the E193 mutation. Methods and Results: First we showed in vitro that the cyclin-dependent kinase inhibitor protein p27kip1 is a direct target of Eya4/Six1 and is suppressed upon Eya4 overexpression, whereas E193 has a dominant negative effect, releasing Eya4 mediated suppression of p27. We next generated transgenic mice with cardiac specific constitutive overexpression of full-length Eya4 or the mutant form E193. While E193 transgenic mice developed age-dependent DCM, Eya4 mice displayed cardiac hypertrophy already under basal conditions as judged by increases in heart weight and cardiomyocyte cross-sectional areas along with increases in myocardial dimension and mass. These two distinct cardiac phenotypes were even more aggravated upon pressure overload suggesting Eya4 is a regulator of cardiac hypertrophy. We also observed that the activity of Casein Kinase 2-α and the phosphorylation status of HDAC2 were significantly upregulated in the Eya4 transgenic mice, while they were significantly reduced in E193 mice, under baseline conditions and pressure overload. We were also able to identify a new human mutation (E215) with a phenotype comparable to the one seen in E193 patients. Conclusion: Our results implicate that Eya4/Six1 regulates cardiac hypertrophic reactions via p27/CK2-α/HDAC2 and indicate that truncating mutations in Eya4 interfere with this newly established signalling pathway.

Corrigendum to: Auxin is required for pollination-induced ovary growth in Dendrobium orchids

2006 ◽  
Vol 33 (10) ◽  
pp. 981 ◽  
Author(s):  
Saichol Ketsa ◽  
Apinya Wisutiamonkul ◽  
Wouter G. van Doorn
Keyword(s):  
Auxin Transport ◽  
Isobutyric Acid ◽  
Signalling Pathway ◽  
Aminooxyacetic Acid ◽  
Ethylene Synthesis ◽  
Transport Inhibitor ◽  
Auxin Signalling ◽  
Auxin Transport Inhibitor ◽  
Ethylene Action ◽  
Ovary Growth

In Dendrobium and other orchids the ovule becomes mature long after pollination, whereas the ovary starts growing within two days of pollination. The signalling pathway that induces rapid ovary growth after pollination has remained elusive. We placed the auxin antagonist �-(p-chlorophenoxy) isobutyric acid (PCIB) or the auxin transport inhibitor 2,3,5-triiodobenzoic acid (TIBA) on the stigma, before pollination. Both treatments nullified pollination-induced ovary growth. The ovaries also did not grow after similar stigma treatment with 1-methylcyclopropene (1-MCP), AgNO3 (both inhibitors of ethylene action), aminooxyacetic acid (AOA) or CoCl2 (which both inhibit ethylene synthesis), before pollination. Pollination could be replaced by placement of the auxin naphthylacetic acid (NAA) on the stigma. All mentioned inhibitors nullified the effect of NAA, indicating that if auxin is the initiator of ovary growth, it acts through ethylene. The results suggest that the pollination effect on ovary growth requires auxin (at least auxin transport and maybe also auxin signalling), and both ethylene synthesis and ethylene action.

The white-tip nematode, Aphelenchoides besseyi, exhibits an auxin-orientated behaviour affecting its migration and propagation

Nematology ◽  
2014 ◽  
Vol 16 (7) ◽  
pp. 837-845 ◽  
Author(s):  
Hui Feng ◽  
Ying Shao ◽  
Li-hui Wei ◽  
Cun-yi Gao ◽  
Yi-jun Zhou
Keyword(s):  
Auxin Transport ◽  
Naphthaleneacetic Acid ◽  
Male Sterile ◽  
Auxin Level ◽  
Rice Plants ◽  
Transport Inhibitor ◽  
Large Numbers ◽  
Auxin Concentration ◽  
Aphelenchoides Besseyi ◽  
Auxin Transport Inhibitor

Aphelenchoides besseyi is an obligate parasite that often causes white-tip symptoms in rice plants. The nematode exhibits ectoparasitic behaviour with its infection rate matching the development of rice plants. Few studies have analysed how A. besseyi migration is influenced by chemical and host factors. Here, we focused on the effects of auxins on nematode migration and propagation. Exposure of A. besseyi to an auxin gradient created by a Pluronic F-127 gel resulted in nematode aggregation at the highest auxin concentration tested, 100 μm. Inoculation on the susceptible cv. Ningjing1 produced more nematodes than on the resistant rice cv. Tetep, which correlated with their endogenous auxin levels. Young panicles treated with 1-naphthaleneacetic acid produced more grains and nematodes, whereas plants treated with the auxin transport inhibitor, 2,3,5-triiodobenzoic acid, led to fewer nematodes in the seeds. In addition, A. besseyi rarely migrated and multiplied in the plants of the male sterile rice cv. Zhenshan97A, which had insufficient auxin level in pollen and thus could not generate any grains in most panicles. However, large numbers of nematodes were observed in seeds of cv. Zhenshan97A that had received pollens from the maintainer cv. Zhenshan97B. The results indicate that auxin might play a key role in the migration and propagation of A. besseyi.

RUNX1/EVI1 That Blocks Myeloid Differentiation Inhibits C/EBPα Function.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 4161-4161
Author(s):  
Katsuya Tokita ◽  
Kazuhiro Maki ◽  
Kinuko Mitani
Keyword(s):  
Dna Binding ◽  
Molecular Mechanisms ◽  
Dominant Negative ◽  
Myelogenous Leukemia ◽  
Dominant Negative Effect ◽  
Granulocytic Differentiation ◽  
Leukemic Transformation ◽  
Hematopoietic Stem ◽  
Differentiation Block ◽  
Myeloid Progenitors

Abstract RUNX1/EVI1 chimeric transcription factor produced by t(3;21) causes leukemic transformation in hematopoietic stem cell tumors such as chronic myelogenous leukemia (CML) in blastic crisis and myelodysplastic syndrome (MDS) in leukemic transformation, possibly through differentiation block of malignant myeloid progenitors. We have recently reported that Runx1/EVI1 knock-in heterozygous mice show defective hematopoiesis in the fetal liver similar to Runx1 knock-out mice, but possess dysplastic hematopoietic progenitors with high self-renewal capacity. Notably, Runx1/EVI1 knock-in chimeric mice developed acute megakaryoblastic leukemia. The molecular characterization of RUNX1/EVI1 points two major functions; one is dominant-suppressive function over wild-type RUNX1 and the other is EVI1’s own function; blockade of TGFb-mediated signal, inhibition of JNK and stimulation of AP-1 activity. C/EBPa is a key transcriptional regulator that induces the granulocytic differentiation of myeloid progenitors and several lines of evidence suggest that disturbance in C/EBPa signaling is one of the major molecular events in myeloid malignancies. In this study, we investigated whether RUNX1/EVI1 affects the expression and function of C/EBPa. We introduced RUNX1/EVI1 cDNA into LG-3 cells that differentiate along the myeloid lineage upon granulocyte colony-stimulating factor exposure, and confirmed that RUNX1/EVI1 suppressed the differentiation. To further investigate the molecular mechanisms of RUNX1/EVI1-mediated differentiation block, we analyzed RUNX1/EVI1’s effect on the functions of C/EBPa. RUNX1/EVI1 was found to associate with C/EBPa. By using the reporter assay with the CEBPA promoter, we observed a dominant-negative effect of RUNX1/EVI1 over C/EBPa-mediated transcriptional activation via the CtBP-binding site in the EVI1 portion. In the gel-shift assay, RUNX1/EVI1 down-regulated DNA-binding activity of C/EBPa. Therefore, recruitment of histone deacetylase via CtBP and disruption of DNA binding could be likely scenarios for the RUNX1/EVI1-induced dominant repression on C/EBPa. Importantly, co-expression of C/EBPa restored differentiation ability of the RUNX1/EVI1-expressing LG-3 cells. All these data argue that inhibition of C/EBPa function may be causatively related to the RUNX1/EVI1’s leukemogenic potential.

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