First Report of Root and Collar Rot Caused by Fusarium tricinctum and Fusarium avenaceum on Carrot in France

In 2017, carrot (Daucus carota L.) seed production represented around 22% of the area devoted to the production of vegetable fine seeds. Since 2015, symptoms of root and collar rot have been observed in carrot seed parcels located in the Central Region, one of the most important production zone in France. Diseased plants became dried prematurely, compromising seed development. Depending on the year and the climatic conditions, the disease in a same field can be considered as epidemic (rate losses between 30 to 100% of plants in 2016) or can impact plants more sporadically (less than 10% in 2017 and 2018). Sixteen diseased carrot samples (Nantaise type) were collected from five fields of seed production in the Central Region: two fields in 2016 and 2017, one field in 2018. Seven fungal isolates, obtained from lesions, were grown on Potato Dextrose Agar (PDA) medium and incubated for one week at 20°C in darkness. From the colony top, fluffy mycelium pigmented in pink, red, purple or orange was observed, with a red color at the reverse. To induce sporulation, isolates were grown on Synthetischer Nährstoffarmer Agar (SNA) medium during three weeks at 24°C in near-UV radiations under a 12h-photoperiod. Four isolates (FT001, FT003, FT007, FT017) developed orange sporodochia with lunar or crescent-shaped macroconidia (40.3 ± 0.8 × 5.9 ± 0.1 µm; n=90) and lime or pear-shaped microconidia (10.7 ± 0.2 × 7.7 ± 0.2 µm; n=60), as described in Fusarium tricinctum (Leslie and Summerell 2006). Three isolates (FA001, FA002, FA006) developed orange sporodochia with sickle-shaped macroconidia (50.5 ± 1.1 × 5.0 ± 0.1 µm; n= 60), but no microconidia, as observed in Fusarium avenaceum (Leslie and Summerell 2006). To confirm the identification, DNA was extracted from the mycelium of the seven isolates and molecular markers (ATP citrate lyase, ACL1; RNA polymerase II, RPB2) were used for PCR amplification (Gräfenhan et al. 2011; O’Donnell et al. 2013). The ACL1 sequences from the seven field isolates (GenBank Accession numbers MK183788-MK183791; MK181528-MK181530) were 99-100% identical with the ACL1 sequence of a reference F. tricinctum isolate (query coverages 99-100%; E-values of 0.0) and a reference F. avenaceum isolate (query coverages 98-99%; E-values of 0.0) [respectively DAOM 235630 isolate, GenBank Acc. No. JX397813 and BBA64135 isolate, GenBank Acc. No. JX397768, Niessen et al. 2012]. Using RPB2, sequences from field isolates (GenBank Acc. No. MK183109-MK183115) were 98.5-99.9% identical with the RPB2 sequence of a reference F. tricinctum isolate (query coverages 96-100%; E-values of 0.0) and a reference F. avenaceum isolate (query coverages 95-100%; E-values of 0.0) [respectively MRC 1895 isolate, GenBank Acc. No. MH582113 and MRC 1413 isolate, GenBank Acc. No. MH582082, O’Donnell et al. 2018]. To confirm pathogenicity, FT001 and FA002 were inoculated on collars of 10-weeks old carrot plants in the greenhouse. Forty plants per isolate and 40 control plants were used. Ten microliters of a conidial suspension (105 conidia.mL-1) - or sterile water for the controls - were deposited at the collar, previously wounded using a scalpel blade. Necrotic lesions developed at 20 dpi (FT001) and at 30 dpi (FA002). Fusarium tricinctum and F. avenaceum were re-isolated from the lesions and identified by sequencing using ACL1 and RPB2 markers. No isolation of Fusarium was obtained from the controls. To our knowledge, this is the first report of F. tricinctum and F. avenaceum in carrot in France

Umbel browning and stem necrosis on carrot seed crop in France: characterization of the fungal pathogen, seed testing and control methods

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Virtual Ontogeny of Cortical Growth Preceding Mental Illness

Background: Morphology of the human cerebral cortex differs across psychiatric disorders, with neurobiology and developmental origins mostly undetermined. Deviations in the tangential growth of the cerebral cortex during pre/perinatal periods may be reflected in individual variations in cortical surface area later in life. Methods: Interregional profiles of group differences in surface area between cases and controls were generated using T1-weighted magnetic resonance imaging from 27,359 individuals including those with attention-deficit/hyperactivity disorder, autism spectrum disorder, bipolar disorder, major depressive disorder, schizophrenia, and high general psychopathology (through the Child Behavior Checklist). Similarity of interregional profiles of group differences in surface area and prenatal cell-specific gene expression was assessed. Results: Across the 11 cortical regions, group differences in cortical area for attention-deficit/hyperactivity disorder, schizophrenia, and Child Behavior Checklist were dominant in multimodal association cortices. The same interregional profiles were also associated with interregional profiles of (prenatal) gene expression specific to proliferative cells, namely radial glia and intermediate progenitor cells (greater expression, larger difference), as well as differentiated cells, namely excitatory neurons and endothelial and mural cells (greater expression, smaller difference). Finally, these cell types were implicated in known pre/perinatal risk factors for psychosis. Genes coexpressed with radial glia were enriched with genes implicated in congenital abnormalities, birth weight, hypoxia, and starvation. Genes coexpressed with endothelial and mural genes were enriched with genes associated with maternal hypertension and preterm birth. Conclusions: Our findings support a neurodevelopmental model of vulnerability to mental illness whereby prenatal risk factors acting through cell-specific processes lead to deviations from typical brain development during pregnancy

Virtual Ontogeny of Cortical Growth Preceding Mental Illness

Background: Morphology of the human cerebral cortex differs across psychiatric disorders, with neurobiology and developmental origins mostly undetermined. Deviations in the tangential growth of the cerebral cortex during pre/perinatal periods may be reflected in individual variations in cortical surface area later in life. Methods: Interregional profiles of group differences in surface area between cases and controls were generated using T1-weighted magnetic resonance imaging from 27,359 individuals including those with attention-deficit/hyperactivity disorder, autism spectrum disorder, bipolar disorder, major depressive disorder, schizophrenia, and high general psychopathology (through the Child Behavior Checklist). Similarity of interregional profiles of group differences in surface area and prenatal cell-specific gene expression was assessed. Results: Across the 11 cortical regions, group differences in cortical area for attention-deficit/hyperactivity disorder, schizophrenia, and Child Behavior Checklist were dominant in multimodal association cortices. The same interregional profiles were also associated with interregional profiles of (prenatal) gene expression specific to proliferative cells, namely radial glia and intermediate progenitor cells (greater expression, larger difference), as well as differentiated cells, namely excitatory neurons and endothelial and mural cells (greater expression, smaller difference). Finally, these cell types were implicated in known pre/perinatal risk factors for psychosis. Genes coexpressed with radial glia were enriched with genes implicated in congenital abnormalities, birth weight, hypoxia, and starvation. Genes coexpressed with endothelial and mural genes were enriched with genes associated with maternal hypertension and preterm birth. Conclusions: Our findings support a neurodevelopmental model of vulnerability to mental illness whereby prenatal risk factors acting through cell-specific processes lead to deviations from typical brain development during pregnancy