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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