Interactions among species with contrasting dispersal modes explain distributions for epiphytic lichens

Understanding how the biodiversity response to climate change will be modified at ecological scales, e.g. by species interactions, is a major challenge. Lichen epiphytes – the close interdependent relationship between a heterotrophic fungus and photosynthetic partner (photobiont) – are used here to explore how interaction regimes (between lichen species, and between lichens and their photobionts) explain distribution patterns along spatial climatic gradients. To do this we tested field evidence for the ‘core‐fringe hypothesis’, which proposes a facilitative interaction; sexually‐reproducing and spore‐dispersed lichens with a requirement for resynthesis with a compatible photobiont (Nostoc) are facilitated by the prior establishment of asexual lichens which disperse both the fungus and photobiont together. We used two closely related Nephroma species which differ in their reproductive mode – N. laevigatum (sexual spore‐dispersed) and N. parile (asexual) – and compared their occurrence along a bioclimatic gradient to local habitat factors, including the co‐occurrence of asexual lichens which have shared specificity for compatible Nostoc genotypes. The results showed that: 1) N. laevigatum is significantly more likely to occur on trees that have already been colonised by asexual lichens with shared specificity for Nostoc, supporting the core‐fringe hypothesis, while 2) N. parile is independent of this association (strengthening the core‐fringe hypothesis), with its response to a precipitation gradient modified by microhabitat factors. This positive test for the core‐fringe hypothesis demonstrates how interaction regimes can fundamentally alter expectations under climate change. There is an assumption that spore‐dispersed lichen species could more easily track their suitable bioclimatic space through fragmented habitat, compared to asexual species with larger and heavier propagules. However, the establishment of spore‐dispersed lichen epiphytes into new habitat may be limited by the dispersal rates of asexual species, which act as key facilitators.     

Severity of Mitral Valve Degeneration Is Associated with Chromosome 15 Loci in Whippet Dogs

Mitral valve degeneration (MVD) is the most common form of heart disease in dogs, frequently leading to left-sided congestive heart failure and cardiac mortality. Although breed-specific disease characteristics and overrepresentation point towards a genetic origin for MVD, a causative mutation and complete molecular pathogenesis are unknown. Whippet dogs are overrepresented in incidence of MVD, suggesting an inherited component in this breed. Expressivity of this condition is variable with some dogs showing evidence of more severe disease at earlier ages than other dogs. This phenomenon makes a traditional case versus control genetic study prone to phenotyping error. This study sought to avoid these common pitfalls by identifying genetic loci associated with severity of MVD in Whippets through a genome-wide association study (GWAS). 138 Whippet dogs were characterized for MVD by echocardiographic examination and a novel disease severity score was developed and adjusted for age in each subject. Single nucleotide polymorphism (SNP) genotype data (170k Illumina CanineHD SnpChip) was obtained for DNA isolated from blood of each study subject. Continuous variable genome wide association was performed after correction for population stratification by efficient mixed model association expedited (EMMAX) in 130 dogs. A genome wide significant association was identified on chromosome 15 (peak locus 57,770,326; P_adj = 0.049) and secondary loci of suggestive association were identified on chromosome 2 (peak locus 37,628,875; P_adj = 0.079). Positional candidate genes were identified within the primary and secondary loci including follistatin-related protein 5 precursor (FSTL5) and Rho GTPase-activating protein 26 (ARHGAP26). These results support the hypothesis that severity of MVD in whippets has a genetic basis and warrants further study by either candidate gene sequencing or next-generation techniques.     

Different Patterns of Agonist-Stimulated Increases of 3H-Inositol Phosphate Isomers and Cytosolic Ca2+ in Bovine Adrenal Chromaffin Cells: Comparison of the Effects of Histamine and Angiotensin II

Abstract: Bovine adrenal chromaffin cells (BCC) were used to compare histamine- and angiotensin II-induced changes of inositol mono-, bis-, and trisphosphate (InsP₁, InsP₂, and InsP₃, respectively) isomers, intracellular free Ca²⁺ ([Ca²⁺]_i), and the pathways of inositol phosphate metabolism. Both agonists elevated [Ca²⁺]_i by 200 nM 3–4 s after addition, but afterwards the histamine response was much more prolonged. Histamine and angiotensin II also produced similar four- to fivefold increases of Ins(1,4,5)P₃ that peaked within 5 s. Over the first minute of stimulation, however, Ins(1,4,5)P₃ formation was monophasic after angiotensin II, but biphasic after histamine, evidence supporting differential regulation of angiotensin II- and histamine-stimulated signal transduction. The metabolism of Ins(1,4,5)P₃ by BCC homogenates was found to proceed via (a) sequential dephosphorylation to Ins(1,4)P₂ and Ins(4)P, and (b) phosphorylation to inositol 1,3,4,5-tetrakisphosphate, followed by dephosphorylation to Ins(1,3,4)P₃, Ins(1,3)P₂, and Ins(3,4)P₂, and finally to Ins(1 or 3)P. In whole cells, Ins(1 or 3)P only increased after histamine treatment. Additionally, Ins(1,3)P₂ was the only other InsP₂ besides Ins(1,4)P₂ to accumulate within 1 min of agonist treatment [Ins(3,4)P₂ did not increase]. These results support a correlation between the time course of Ins(1,4,5)P₃ formation and the time course of [Ca²⁺]_i transients and illustrate that Ca²⁺-mobilizing agonists can produce distinguishable patterns of inositol phosphate formation and [Ca²⁺], changes in BCC. Different patterns of second-messenger formation are likely to be important in signal recognition and may encode agonist-specific information.     

Origins and patterns of endemic diversity in two specialized lizard lineages from the Australian Monsoonal Tropics (Oedura spp.)

Aim

Savanna biomes cover around 20% of land surfaces, yet the origins and processes that have shaped their biodiversity remain understudied. Here, we assess the timing of diversification and how patterns of genetic diversity vary along an aridity gradient in specialized saxicoline gecko clades (Oedura spp.) from the tropical savannas of northern Australia.

Location

Australian Monsoonal Tropics (AMT), Kimberley region (Western Australia).

Methods

We compiled mitochondrial and nuclear data for two Kimberley endemic lizard clades (Oedura filicipoda/murrumanu and O. gracilis), and allied non‐Kimberley taxa (O. marmorata complex). Species delimitation methods were used to identify evolutionary lineages, Maximum‐likelihood and Bayesian phylogenetic methods were employed to assess relationships and diversification timeframes, and rainfall data and range sizes were tested for correlations.

Results

Phylogenetic analyses of cryptic or recently discovered lineage diversity revealed late‐Miocene to early‐Pliocene crown ages. Microendemism and diversity were highest in high‐rainfall regions, while the most widespread lineages occurred in the central and south‐east Kimberley, and showed evidence of introgression with parapatric lineages.

Main conclusions

The initial diversification in both clades was broadly concordant with global climatic events linked to the expansion of savanna biomes in the lateMiocene. Higher endemism in mesic and refugial areas suggests long histories of localized persistence, while wider distributions and evidence of introgression suggest a dynamic history at the arid‐monsoonal interface.     

EPA,not DHA,prevents fibrosis in pressure overload-induced heart failure: potential role of free fatty acid receptor 4

Heart failure with preserved ejection fraction (HFpEF) is half of all HF, but standard HF therapies are ineffective. Diastolic dysfunction, often secondary to interstitial fibrosis, is common in HFpEF. Previously, we found that supra-physiologic levels of ω3-PUFAs produced by 12 weeks of ω3-dietary supplementation prevented fibrosis and contractile dysfunction following pressure overload [transverse aortic constriction (TAC)], a model that resembles aspects of remodeling in HFpEF. This raised several questions regarding ω3-concentration-dependent cardioprotection, the specific role of EPA and DHA, and the relationship between prevention of fibrosis and contractile dysfunction. To achieve more clinically relevant ω3-levels and test individual ω3-PUFAs, we shortened the ω3-diet regimen and used EPA- and DHA-specific diets to examine remodeling following TAC. The shorter diet regimen produced ω3-PUFA levels closer to Western clinics. Further, EPA, but not DHA, prevented fibrosis following TAC. However, neither ω3-PUFA prevented contractile dysfunction, perhaps due to reduced uptake of ω3-PUFA. Interestingly, EPA did not accumulate in cardiac fibroblasts. However, FFA receptor 4, a G protein-coupled receptor for ω3-PUFAs, was sufficient and required to block transforming growth factor β1-fibrotic signaling in cultured cardiac fibroblasts, suggesting a novel mechanism for EPA. In summary, EPA-mediated prevention of fibrosis could represent a novel therapy for HFpEF.