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Acquisition of enemy-free-space has been suggested to reduce selective pressure against host range expansion in phytophagous insects. The gall midge, Asphondylia borrichiae Rossi and Strong (Diptera: Cecidomyiidae), which attacks the stem tips of its 3 host plants produces a spherical tumor-like growth (= gall). Juvenile stages (larvae and pupae) of A. borrichiae develop inside the gall; the midge spends approximately 95-98% of its life cycle embedded within the gall. During these juvenile stages, A. borrichiae are parasitized by 4 species of hymenopterans. Previous studies have found that one of the most common and the largest parasitoid, Torymus umbilicatus (Gahan), tends to dominate large galls owing to its significantly longer ovipositor, which enables it to penetrate the biggest galls and reach larvae and pupae that become unavailable to the other 3 parasitoids, which have much shorter ovipositors. Moreover, previous studies suggest that the gall midge is diverging both morphologically and genetically in sympatry. The current study is the first to provide morphological evidence that T. umbilicatus, which is a dominant member of the parasitoid guild that attacks A. borrichiae, may also be diverging in sympatry along with its host. Female T. umbilicatus from sea oxeye daisy (Borrichia frutescens [L.] DC) were significantly larger than those from alternative host plants of the gall midge, dune elder (Iva imbricata Walter) and marsh elder (I. frutescens L). Additionally, size of female T. umbilicatus collected from 2 geographically distant sites were significantly different and these differences were consistent with a latitudinal gradient in size between plant species. Although T. umbilicatus were larger from galls collected from B. frutescens compared to I. frutescens at both sites, gall diameter demonstrated a significant decline along a south-north latitudinal gradient. However, a significant interaction between plant species and site suggests that differences in T. umbilicatus size (and most likely their gall midge host) is caused either by phenotypic plasticity of the species at the 2 sites, or these insects (T. umbilicatus and gall midges) tend to be smaller with increasing latitude. Moreover, galls on I. frutescens, owing to their smaller size and increased crowding, decline in size at a greater rate than those from B. frutescens which produces significantly larger and less crowded galls. [ABSTRACT FROM AUTHOR]

Summary: Background: Hexanucleotide repeat expansions in chromosome 9 open reading frame 72 (C9ORF72) are the most common known genetic cause of frontotemporal dementia (FTD) and motor neuron disease (MND). We assessed whether expansion size is associated with disease severity or phenotype. Methods: We did a cross-sectional Southern blot characterisation study (Xpansize-72) in a cohort of individuals with FTD, MND, both these diseases, or no clinical phenotype. All participants had GGGGCC repeat expansions in C9ORF72, and high quality DNA was available from one or more of the frontal cortex, cerebellum, or blood. We used Southern blotting techniques and densitometry to estimate the repeat size of the most abundant expansion species. We compared repeat sizes between different tissues using Wilcoxon rank sum and Wilcoxon signed rank tests, and between disease subgroups using Kruskal-Wallis rank sum tests. We assessed the association of repeat size with age at onset and age at collection using a Spearman's test of correlation, and assessed the association between repeat size and survival after disease onset using Cox proportional hazards regression models. Findings: We included 84 individuals with C9ORF72 expansions: 35 had FTD, 16 had FTD and MND, 30 had MND, and three had no clinical phenotype. We focused our analysis on three major tissue subgroups: frontal cortex (available from 41 patients [21 with FTD, 11 with FTD and MND, and nine with MND]), cerebellum (40 patients [20 with FTD, 12 with FTD and MND, and eight with MND]), and blood (47 patients [15 with FTD, nine with FTD and MND, and 23 with MND] and three carriers who had no clinical phenotype). Repeat lengths in the cerebellum were smaller (median 12·3 kb [about 1667 repeat units], IQR 11·1–14·3) than those in the frontal cortex (33·8 kb [about 5250 repeat units], 23·5–44·9; p<0·0001) and those in blood (18·6 kb [about 2717 repeat units], 13·9–28·1; p=0·0002). Within these tissues, we detected no difference in repeat length between disease subgroups (cerebellum p=0·96, frontal cortex p=0·27, blood p=0·10). In the frontal cortex of patients with FTD, repeat length correlated with age at onset (r=0·63; p=0·003) and age at sample collection (r=0·58; p=0·006); we did not detect such a correlation in samples from the cerebellum or blood. When assessing cerebellum samples from the overall cohort, survival after disease onset was 4·8 years (IQR 3·0–7·4) in the group with expansions greater than 1467 repeat units (the 25th percentile of repeat lengths) versus 7·4 years (6·3–10·9) in the group with smaller expansions (HR 3·27, 95% CI 1·34–7·95; p=0·009). Interpretation: We detected substantial variation in repeat sizes between samples from the cerebellum, frontal cortex, and blood, and longer repeat sizes in the cerebellum seem to be associated with a survival disadvantage. Our findings indicate that expansion size does affect disease severity, which—if replicated in other cohorts—could be relevant for genetic counselling. Funding: The ALS Therapy Alliance, the National Institute of Neurological Disorders and Stroke, the National Institute on Aging, the Arizona Department of Health Services, the Arizona Biomedical Research Commission, and the Michael J Fox Foundation for Parkinson's Research. [Copyright &y& Elsevier]