Summary Plants interact with root microbes via chemical signaling, which modulates competence or symbiosis. Although several volatile organic compounds (VOCs) from fungi may affect plant growth and development, the signal transduction pathways mediating VOC sensing are not fully understood. 6‐pentyl‐2H‐pyran‐2‐one (6‐PP) is a major VOC biosynthesized by Trichoderma spp. which is probably involved in plant–fungus cross‐kingdom signaling. Using microscopy and confocal imaging, the effects of 6‐PP on root morphogenesis were found to be correlated with DR5:GFP, DR5:VENUS, H2B::GFP, PIN1::PIN1::GFP, PIN2::PIN2::GFP, PIN3::PIN3::GFP and PIN7::PIN7::GFP gene expression. A genetic screen for primary root growth resistance to 6‐PP in wild‐type seedlings and auxin‐ and ethylene‐related mutants allowed identification of genes controlling root architectural responses to this metabolite. Trichoderma atroviride produced 6‐PP, which promoted plant growth and regulated root architecture, inhibiting primary root growth and inducing lateral root formation. 6‐PP modulated expression of PIN auxin‐transport proteins in a specific and dose‐dependent manner in primary roots. TIR1, AFB2 and AFB3 auxin receptors and ARF7 and ARF19 transcription factors influenced the lateral root response to 6‐PP, whereas EIN2 modulated 6‐PP sensing in primary roots. These results indicate that root responses to 6‐PP involve components of auxin transport and signaling and the ethylene‐response modulator EIN2.

Low phosphate (Pi) availability constrains plant development and seed production in both natural and agricultural ecosystems. When Pi is scarce, modifications of root system architecture (RSA) enhance the soil exploration ability of the plant and lead to an increase in Pi uptake. In Arabidopsis, an iron-dependent mechanism reprograms primary root growth in response to low Pi availability. This program is activated upon contact of the root tip with low-Pi media and induces premature cell differentiation and the arrest of mitotic activity in the root apical meristem, resulting in a short-root phenotype. However, the mechanisms that regulate the primary root response to Pi-limiting conditions remain largely unknown. Here we report on the isolation and characterization of two low-Pi insensitive mutants (lpi5 and lpi6), which have a long-root phenotype when grown in low-Pi media. Cellular, genomic, and transcriptomic analysis of low-Pi insensitive mutants revealed that the genes previously shown to underlie Arabidopsis Al tolerance via root malate exudation, known as SENSITIVE TO PROTON RHIZOTOXICITY (STOP1) and ALUMINUM ACTIVATED MALATE TRANSPORTER 1 (ALMT1), represent a critical checkpoint in the root developmental response to Pi starvation in Arabidopsis thaliana. Our results also show that exogenous malate can rescue the long-root phenotype of lpi5 and lpi6. Malate exudation is required for the accumulation of Fe in the apoplast of meristematic cells, triggering the differentiation of meristematic cells in response to Pi deprivation.

Low phosphate (Pi) availability constrains plant development and crop production in both natural and agricultural ecosystems. When Pi is scarce, modifications of root system architecture (RSA) enhance soil exploration ability and can lead to an increase in Pi uptake. In Arabidopsis, an iron-dependent determinate developmental program that induces premature differentiation in the root apical meristem (RAM) begins when the root tip contacts low Pi media, resulting in a short-root phenotype. However, the mechanisms that enable the regulation of root growth in response to Pi-limiting conditions remain largely unknown. Cellular, genomic and transcriptomic analysis of low-Pi insensitive mutants revealed that the malate-exudation related genes SENSITIVE TO PROTON RHIZOTOXICITY (STOP1) and ALUMINUM ACTIVATED MALATE TRANSPORTER 1 (ALMT1) represent a critical checkpoint in the root developmental response to Pi starvation in Arabidopsis thaliana.

Arabidopsis MAP kinases are considered to have redundant functions. However, through a detailed phenotypic analysis, we demonstrated that MPK6 loss-of- function cause severe defects in embryo development, which are closed related with alterations in post-germination root development

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Alkamides are small bioactive lipid signals with a wide distribution in plants. In this report, the role of nitric oxide (NO) in the alterations induced by N-isobutyl decanamide on the Arabidopsis (Arabidopsis thaliana) root system architecture (RSA) was investigated. We first compared the effects of N-isobutyl decanamide and NO donors sodium nitropruside (SNP) and S-nitroso-N-acetylpenicillamine (SNAP) on root morphogenetic processes. Both N-isobutyl decanamide and NO donors modulated RSA in a similar way and in a dose-dependent manner, inhibiting primary root growth and promoting lateral root primordia (LRP) formation. RSA alterations induced by N-isobutyl decanamide correlated with NO accumulation in the primary root tip and in developing lateral roots. Morphogenetic effects of N-isobutyl decanamide decreased when NO scavengers were supplied to alkamide-treated seedlings. N-Isobutyl decanamide-regulated root architectural changes were also investigated in mutants defective in NO biosynthesis, nia1 nia2, and NO signalling, Atnoa1, and in the alkamide-resistant mutant drr1. The nia1 nia2 and Atnoa1 mutants were indistinguishable in primary root growth inhibition by the alkamide when compared with wild-type (WT) seedlings, but showed reduced lateral root responses. The drr1 mutant was less sensitive in both primary root growth inhibition and LRP induction by NO donors than WT seedlings. Detailed DR5:uidA and BA3:uidA marker analysis showed that N-isobutyl decanamide and its interacting signals jasmonic acid and NO act downstream or independently of auxin-responsive gene expression to promote LRP formation. Our results provide compelling evidence that NO is an intermediate in alkamide signaling mediating RSA adjustment in Arabidopsis.

Alkamides are fatty acid amides of wide distribution in plants, structurally related to N-acyl-L-homoserine lactones (AHLs) from Gram-negative bacteria and to N- acylethanolamines (NAEs) from plants and mammals. Global analysis of gene expression changes in Arabidopsis thaliana in response to N-isobutyl decanamide, the most highly active alkamide identified to date, revealed an overrepresentation of defense-responsive transcriptional networks. In particular, genes encoding enzymes for jasmonic acid (JA) biosynthesis increased their expression, which occurred in parallel with JA, nitric oxide (NO) and H2O2 accumulation. The activity of the alkamide to confer resistance against the necrotizing fungus Botrytis cinerea was tested by inoculating Arabidopsis detached leaves with conidiospores and evaluating disease symptoms and fungal proliferation. N-isobutyl decanamide application significantly reduced necrosis caused by the pathogen and inhibited fungal proliferation. Arabidopsis mutants jar1 and coi1 altered in JA signaling and a MAP kinase mutant (mpk6), unlike salicylic acid- (SA) related mutant eds16/sid2-1, were unable to defend from fungal attack even when N-isobutyl decanamide was supplied, indicating that alkamides could modulate some necrotrophic-associated defense responses through JA-dependent and MPK6-regulated signaling pathways. Our results suggest a role of alkamides in plant immunity induction.

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.