Litchi (Litchi chinensis) pepper spot disease results in black spotting symptoms on litchi fruits. This disease was first observed on litchi cultivar Guiwei, in Guangzhou, China, in 2009, and then found widespread in other litchi‐growing regions of China. Colletotrichum isolates were consistently recovered from typical black spot lesions of diseased fruits with frequency ranging from 83% to 100%. Three representative Colletotrichum isolates from Maoming, Guangzhou and Shenzhen were selected for identification and pathogenicity testing in the field. Based on morphology and phylogenetic analysis using the ribosomal internal transcribed spacer region (ITS), glyceraldehyde‐3‐phosphate dehydrogenase (GAPDH), calmodulin (CAL), actin (ACT), β‐tubulin (TUB2) and glutamine synthetase (GS) gene sequences, the three isolates were identified as C. siamense. In the pathogenicity experiments, typical symptoms appeared on the inoculated litchi fruits, including black spots and green patches around these black spots. These symptoms were consistent with the symptoms originally observed in the field. Colletotrichum siamense was successfully reisolated from the typical black spot lesions of the inoculated litchi fruits. To the authors' knowledge, this is the first report on characterization of C. siamense as the causal agent of litchi pepper spot disease in mainland China by successful inoculation on fruits under field conditions.
High throughput sequencing was used to reveal the distribution of whole-genome variations in cultivated Morella rubra (Sieb. et Zucc.). A total of 3,151,123 SNPs, 371,757 small indels, and 15,904 SVs were detected in 52 accessions. Verification by Sanger sequencing demonstrated that the positive rate of the SNPs was approximately 97.3%. Search for more genetic variations was expanded to 141 red bayberry accessions, most of which were cultivars, by sequencing 19 selected genomic segments (SEG1-19). The results showed that each segment harbored, on average, 7.8 alleles (haplotypes), a haplotype diversity of 0.42, and a polymorphic information content (PIC) of 0.40. Seventy-two different genotypes were identified from the 141 accessions, and statistical analysis showed that the accessions with duplicated genotypes were either somatic mutants or simply synonyms. Core set selection results showed that a minimum of 34 genotypes could already have covered all the alleles on the segments. A DNA fingerprinting system was developed for red bayberry, which used the diversity information of only 8 DNA segments yet still achieved a very high efficiency without losing robustness. No large clade was robustly supported by hierarchical clustering, and well-supported small clusters mainly included close relatives. These results should lead to an improved understanding of the genetic diversity of red bayberry and be valuable for future molecular breeding and variety protection.
Fusarium species have been identified as pathogens causing many different plant diseases, and here we report an emerging banana leaf blight (BLB) caused by F. sacchari (Fs) discovered in Guangdong, China. From the symptomatic tissues collected in the field, a fungal isolate was obtained, which induced similar symptoms on healthy banana seedlings after inoculation. Koch’s postulates were fulfilled after the re-isolation of the pathogen. Phylogenetic analysis on two gene segments and the whole genome sequence identified the pathogen belonging to Fs and named as Fs str. FS66. A 45.74 Mb genome of FS66 was acquired through de novo assembly using long-read sequencing data, and its contig N50 (1.97 Mb) is more than 10-fold larger than the previously available genome in the species. Based on transcriptome sequencing and ab initio gene annotation, a total of 14,486 protein-encoding genes and 418 non-coding RNAs were predicted. A total of 48 metabolite biosynthetic gene clusters including the fusaric acid biosynthesis gene cluster were predicted in silico in the FS66 genome. Comparison between FS66 and other 11 Fusarium genomes identified tens to hundreds of genes specifically gained and lost in FS66, including some previously correlated with Fusarium pathogenicity. The FS66 genome also harbors widespread gene transfer on the core chromosomes putatively from F. oxysporum species complex (FOSC), including 30 involved in Fusarium pathogenicity/virulence. This study not only reports the BLB caused by Fs, but also provides important information and clues for further understanding of the genome evolution among pathogenic Fusarium species.
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