Knowledge of the relationships and thus the classification of fungi, has developed rapidly with increasingly widespread use of molecular techniques, over the past 10–15 years, and continues to accelerate. Several genera have been found to be polyphyletic, and their generic concepts have subsequently been emended. New names have thus been introduced for species which are phylogenetically distinct from the type species of particular genera. The ending of the separate naming of morphs of the same species in 2011, has also caused changes in fungal generic names. In order to facilitate access to all important changes, it was desirable to compile these in a single document. The present article provides a list of generic names of Ascomycota (approximately 6500 accepted names published to the end of 2016), including those which are lichen-forming. Notes and summaries of the changes since the last edition of ‘Ainsworth & Bisby’s Dictionary of the Fungi’ in 2008 are provided. The notes include the number of accepted species, classification, type species (with location of the type material), culture availability, life-styles, distribution, and selected publications that have appeared since 2008. This work is intended to provide the foundation for updating the ascomycete component of the “Without prejudice list of generic names of Fungi” published in 2013, which will be developed into a list of protected generic names. This will be subjected to the XIXth International Botanical Congress in Shenzhen in July 2017 agreeing to a modification in the rules relating to protected lists, and scrutiny by procedures determined by the Nomenclature Committee for Fungi (NCF). The previously invalidly published generic names Barriopsis, Collophora (as Collophorina), Cryomyces, Dematiopleospora, Heterospora (as Heterosporicola), Lithophila, Palmomyces (as Palmaria) and Saxomyces are validated, as are two previously invalid family names, Bartaliniaceae and Wiesneriomycetaceae. Four species of Lalaria, which were invalidly published are transferred to Taphrina and validated as new combinations. Catenomycopsis Tibell & Constant. is reduced under Chaenothecopsis Vain., while Dichomera Cooke is reduced under Botryosphaeria Ces. & De Not. (Art. 59).

Anthracnose disease caused by Colletotrichum species is a major constraint for the shelf-life and marketability of avocado fruits. To date, only C. gloeosporioides sensu lato and C. aenigma have been reported as pathogens affecting avocado in Israel. This study was conducted to identify and characterize Colletotrichum species associated with avocado anthracnose and to determine their survival on different host-structures in Israel. The pathogen survived and over-wintered mainly on fresh and dry leaves, as well as fresh twigs in the orchard. A collection of 538 Colletotrichum isolates used in this study was initially characterized based on morphology and banding patterns generated according to arbitrarily primed PCR to assess the genetic diversity of the fungal populations. Thereafter, based on multi-locus phylogenetic analyses involving combinations of ITS, act, ApMat, cal, chs1, gapdh, gs, his3, tub2 gene/markers; eight previously described species (C. aenigma, C. alienum, C. fructicola, C. gloeosporioides sensu stricto, C. karstii, C. nupharicola, C. siamense, C. theobromicola) and a novel species (C. perseae) were identified, as avocado anthracnose pathogens in Israel; and reconfirmed after pathogenicity assays. Colletotrichum perseae sp. nov. and teleomorph of C. aenigma are described along with comprehensive morphological descriptions and illustrations, for the first time in this study.

Anthracnose disease caused by the Colletotrichum gloeosporioides species complex is a major problem worldwide. In this study, we investigated the phylogenetic diversity of 207 Indian Colletotrichum isolates, associated with symptomatic and asymptomatic tissues of mango, belonging to this species complex. Phylogenetic analyses were performed based on a 6-gene dataset (act, cal, chs1, gapdh, ITS and tub2), followed by ApMat sequence-analysis. The ApMat-based phylogeny was found to be superior as it provided finer resolution in most of the species-level clades. Importantly, the ApMat marker identified seven lineages within C. siamense sensu lato, including C. jasmini-sambac, C. hymenocallidis, C. melanocaulon, C. siamense sensu stricto and three undesignated, potentially novel lineages. In this study, C. fragariae sensu stricto, C. fructicola, C. jasmini-sambac, C. melanocaulon and five undesignated, potentially novel lineages were found to be associated with mango tissues. There is a need to develop a consensus among mycologists as to which genes should be used to define and delimit a Colletotrichum species and in the mean time mycologists should voluntarily restrain from describing new species based on inadequate datasets.

Colletotrichum gloeosporioides sensu lato has been associated with anthracnose in diverse commercial crops. It is now established that C. gloeosporioides sensu lato comprises 33 phylogenetic species and C. gloeosporioides sensu stricto is not a common pathogen of tropical fruits. In this study, we investigated the phylogenetic relationships of 85 Colletotrichum isolates associated with select tropical fruits and flowering plants from India. In the ApMat marker analysis, the 85 isolates clustered with 7 known Colletotrichum species (C. aotearoa, C. dianesei, C. endomangiferae, C. musae, C. siamense, C. theobromicola, Glomerella cingulata f. sp. camelliae) and six novel lineages. One of the novel lineages is described and illustrated in this paper as Colletotrichum communis sp. nov., while new-host pathogen associations for C. aotearoa, C. endomangiferae, C. dianesei and C. theobromicola are reported from India. Out of the 85 isolates analysed in this paper, 73 isolates clustered within the C. siamense species complex, indicating that C. siamense species complex, not C. gloeosporioides sensu stricto, is common on tropical fruits. In comparison with act, cal, gapdh, ITS and tub2 gene markers, we recommend the use of the ApMat marker for accurate identification of cryptic species within the C. siamense species complex. We believe that the ApMat marker, in combination with one or two similar ‘phylogenetically superior’ gene markers, is a better candidate for species-level classification of fungi that were traditionally identified as ‘Colletotrichum gloeosporioides’.

Summary: Pea powdery mildew (PM) is an important fungal disease caused by an obligate biotroph, Erysiphe pisi ( Ep ), which significantly impacts pea production worldwide. The phytopathogen secretes a plethora of effectors, primarily through specialized infection structures termed haustoria, to establish a dynamic relationship with its host. To identify Ep effector candidates, a cDNA library of enriched haustoria from Ep ‐infected pea leaves was sequenced. The Ep transcriptome encodes 622 Ep candidate secreted proteins (CSPs), of which 167 were predicted to be candidate secreted effector proteins (CSEPs). Phylogenetic analysis indicates that Ep CSEPs are highly diverse, but, unlike cereal PM CSEPs, exhibit extensive sequence similarity with effectors from other PMs. Quantitative real‐time PCR of a subset of EpCSEP / CSPs revealed that the majority are preferentially expressed in haustoria and exhibit infection stage–specific expression patterns. The functional roles of EpCSEP001 , EpCSEP009 and EpCSP083 were probed by host‐induced gene silencing (HIGS) via a double‐stranded (ds) RNA‐mediated RNAi approach. Foliar application of individual EpCSEP / CSP dsRNAs resulted in a marked reduction in PM disease symptoms. These findings were consistent with microscopic and molecular studies, suggesting that these Ep CSEP/CSPs play important roles in pea PM pathogenesis. Homology modelling revealed that Ep CSEP001 and Ep CSEP009 are analogous to fungal ribonucleases and belong to the RALPH family of effectors. This is the first study to identify and functionally validate candidate effectors from the agriculturally relevant pea PM, and highlights the utility of transcriptomics and HIGS to elucidate the key proteins associated with Ep pathogenesis.