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In subarctic mountain birch forests, reindeer grazing and moth outbreaks act as important biotic drivers of ecosystem functioning. We investigated how a long-term contrast in reindeer grazing regimes and short-term ungulate exclusion affected soil fungal and bacterial communities in mountain birch forests recovering from a recent moth outbreak. We separately described the impacts on microbial communities for organic and mineral soil layers. Differences in fungal communities were mainly explained by variations between grazing regimes, whereas the four-year exclusion of ungulates had little effect. Soil microbial communities showed a high level of specificity between organic and mineral layers. Our results suggest that long-term grazing may have cascading impacts, especially on ectomycorrhizal fungal communities. In contrast, ericoid mycorrhizal and saprotrophic fungal communities and soil bacterial communities were less affected by grazing and appeared to be more resilient to aboveground herbivory in mountain birch forests recovering from a moth outbreak. [ABSTRACT FROM AUTHOR]

American Cocker Spaniels (ACSs) develop aural ceruminous gland hyperplasia and ectasia more often than dogs of other breeds. Data on the cause and development of these breed characteristic histopathological changes are lacking. We performed video-otoscopic examinations and dermatological work-up on 28 ACSs, obtained aural biopsies from each dog and assessed the statistical associations between the presence of ceruminous gland hyperplasia and ectasia and disease history, clinical or microbiological findings and underlying cause of otitis externa (OE). Histological lesions of ceruminous gland hyperplasia and ectasia were observed in aural biopsies from 6/13 clinically healthy ears and 13/15 ears with OE from 19/28 examined dogs. Nine of 28 dogs had histologically normal ceruminous glands (odds ratio [OR] 6.2, 95% confidence interval [CI] 1.1–36.6). Bacterial growth in microbiological culture of aural exudate (OR 14.1, 95% CI 2.1–95.3) was associated with ceruminous glandular changes, whereas previous history of OE, cutaneous findings or underlying allergies were not. Pedigree analysis and a genome-wide association study (GWAS) were performed on 18 affected and eight unaffected dogs based on histopathological diagnosis. While the GWAS indicated a tentative, but not statistically significant, association of ceruminous gland hyperplasia and ectasia with chromosome 31, a larger cohort is needed to confirm this preliminary result. Based on our results, ceruminous gland hyperplasia and ectasia may also precede clinical signs of OE in ACSs and a genetic aetiological component is likely Further studies with larger cohorts are warranted to verify our preliminary results. [ABSTRACT FROM AUTHOR]

Summary Maternally skewed transmission of traits has been associated with genomic imprinting and oocyte-derived mRNA. We report canine congenital eye malformations, caused by an amino acid deletion (K12del) near the N terminus of retinol-binding protein ( RBP4 ). The disease is only expressed when both dam and offspring are deletion homozygotes. RBP carries vitamin A (retinol) from hepatic stores to peripheral tissues, including the placenta and developing eye, where it is required to synthesize retinoic acid. Gestational vitamin A deficiency is a known risk factor for ocular birth defects. The K12del mutation disrupts RBP folding in vivo , decreasing its secretion from hepatocytes to serum. The maternal penetrance effect arises from an impairment in the sequential transfer of retinol across the placenta, via RBP encoded by maternal and fetal genomes. Our results demonstrate a mode of recessive maternal inheritance, with a physiological basis, and they extend previous observations on dominant-negative RBP4 alleles in humans. [ABSTRACT FROM AUTHOR]

• The two-way dependency of streams and their riparian forests is reviewed. • We focus on biodiversity and ecosystem functions, including microbial processes. • Land use and climate change effects on riparian and stream ecosystems are discussed. • Potential management and protection practices are overviewed. • Future research questions are drawn together. In this review, we draw together the research on the two-way connection of streams and their riparian forests of the boreal zone from ecological points of view. Although the knowledge about stream-riparian interactions has increased considerably recently, in practice, riparian zones are still mainly seen as buffers for nutrient and sediment loading. However, recent research has shown that riparian forests disproportionately foster regional biodiversity and maintain stream ecosystem functions and diversity. On the other hand, streams contribute to riparian diversity and ecosystem functions. Microbes are key drivers of global biochemical cycles, and they also interact with plants and animals. The knowledge on microbial communities and understanding of processes they drive has considerably increased due to recent development in microbial profiling methods. However, microbes have been largely neglected in former reviews. Thus, this overview has a special focus on the role of microorganisms in controlling stream-riparian interaction. We also review the land-use pressures that are threatening biodiversity and ecosystem processes of riparian zones in forested landscapes. In addition, we review the possible effects of climate change on stream-riparian interactions. Finally, we outline the research gaps that call for future research. [ABSTRACT FROM AUTHOR]

The soluble α-polyglucan glycogen is a central metabolite enabling transient glucose storage to suit cellular energy needs. Glycogen storage diseases (GSDs) comprise over 15 entities caused by generalized or tissue-specific defects in enzymes of glycogen metabolism. In several, e.g. in Lafora disease caused by the absence of the glycogen phosphatase laforin or its interacting partner malin, degradation-resistant abnormally structured insoluble glycogen accumulates. Sensitive quantification methods for soluble and insoluble glycogen are critical to research, including therapeutic studies, in such diseases. This paper establishes methodological advancements relevant to glycogen metabolism investigations generally, and GSDs. Introducing a pre-extraction incubation method, we measure degradation-resistant glycogen in as little as 30 mg skeletal muscle or a single hippocampus from Lafora disease mouse models. The digestion-resistant glycogen correlates with the disease-pathogenic insoluble glycogen and can readily be detected in very young mice where glycogen accumulation has just begun. Secondly, we establish a high-sensitivity glucose assay with detection of ATP depletion, enabling 1) quantification of α-glucans in cell culture using a medium-throughput assay suitable for assessment of candidate glycogen synthesis inhibitors, and 2) discovery of α-glucan material in healthy human cerebrospinal fluid, establishing a novel methodological platform for biomarker analyses in Lafora disease and other GSDs. [ABSTRACT FROM AUTHOR]

Malstructured glycogen accumulates over time in Lafora disease (LD) and precipitates into Lafora bodies (LBs), leading to neurodegeneration and intractable fatal epilepsy. Constitutive reduction of glycogen synthase-1 (GYS1) activity prevents murine LD, but the effect of GYS1 reduction later in disease course is unknown. Our goal was to knock out Gys1 in laforin (Epm2a)- deficient LD mice after disease onset to determine whether LD can be halted in midcourse, or even reversed. We generated Epm2a-deficient LD mice with tamoxifen-inducible Cre-mediated Gys1 knockout. Tamoxifen was administered at 4 months and disease progression assessed at 12 months. We verified successful knockout at mRNA and protein levels using droplet digital PCR and Western blots. Glycogen determination and periodic acid-Schiff-diastase staining were used to analyze glycogen and LB accumulation. Immunohistochemistry using astrocytic (glial fibrillary acidic protein) and microglial (ionized calcium-binding adapter molecule 1) markers was performed to investigate neuroinflammation. In the disease-relevant organ, the brain, Gys1 mRNA levels were reduced by 85% and GYS1 protein depleted. Glycogen accumulation was halted at the 4-month level, while LB formation and neuroinflammation were significantly, though incompletely, prevented. Skeletal muscle analysis confirmed that Gys1 knockout inhibits glycogen and LB accumulation. However, tamoxifen-independent Cre recombination precluded determination of disease halting or reversal in this tissue. Our study shows that Gys1 knockdown is a powerful means to prevent LD progression, but this approach did not reduce brain glycogen or LBs to levels below those at the time of intervention. These data suggest that endogenous mechanisms to clear brain LBs are absent or, possibly, compromised in laforindeficient murine LD. [ABSTRACT FROM AUTHOR]