New and Interesting Fungi. 1

This study introduces two new families, one new genus, 22 new species, 10 new combinations, four epitypes, and 16 interesting new host and / or geographical records. Cylindriaceae (based on Cylindrium elongatum) is introduced as new family, with three new combinations.Xyladictyochaetaceae (based on Xyladictyochaetalusitanica) is introduced to accommodate Xyladictyochaeta. Pseudoanungitea gen. nov. (based on P.syzygii)is described on stems of Vaccinium myrtillus(Germany). New species include: Exophiala eucalypticola on Eucalyptus obliqua leaf litter, Phyllosticta hakeicola on leaves of Hakea sp.,Setophaeosphaeriacitricola on leaves of Citrus australasica, and Sirastachyscyperacearum on leaves of Cyperaceae(Australia); Polyscytalum chilense on leaves of Eucalyptus urophylla (Chile); Pseudoanungitea vaccinii on Vaccinium myrtillus (Germany); Teichospora quercus on branch tissue of Quercus sp. (France); Fusiconidiumlycopodiellae on stems of Lycopodiella inundata,Monochaetiajunipericola on twig of Juniperus communis,Myrmecridiumsorbicola on branch tissues of Sorbus aucuparia, Parathyridariaphiladelphi on twigs of Philadelphus coronarius, and Wettsteininaphiladelphi on twigs of Philadelphus coronarius (Germany); Zygosporium pseudogibbum on leaves of Eucalyptus pellita (Malaysia); Pseudoanungiteavariabilis on dead wood (Spain); Alfaria acaciae on leaves of Acacia propinqua, Dictyochaeta mimusopis on leaves of Mimusops caffra,and Pseudocercosporabreonadiae on leaves of Breonadia microcephala (South Africa); Colletotrichumkniphofiae on leaves of Kniphofia uvaria,Subplenodomusiridicola on Iris sp., and Trochila viburnicola on twig cankers on Viburnum sp. (UK); Polyscytalum neofecundissimum on Quercus robur leaf litter, and Roussoellaeuonymi on fallen branches of Euonymus europaeus (Ukraine). New combinations include: Cylindrium algarvense on leaves of Eucalyptus sp. (Portugal), Cylindrium purgamentum on leaf litter (USA), Cylindrium syzygii on leaves of Syzygium sp. (Australia), Microdochium musae on leaves of Musa sp. (Malaysia), Polyscytalum eucalyptigenum on Eucalyptus grandis × pellita (Malaysia), P. eucalyptorum on leaves of Eucalyptus (Australia), P. grevilleae on leaves of Grevillea (Australia), P. nullicananum on leaves of Eucalyptus (Australia), Pseudoanungiteasyzygii on Syzygium cordatum leaf litter (South Africa), and Setophaeosphaeriasidae on leaves of Sida sp. (Brazil). New records include: Sphaerellopsis paraphysata on leaves of Phragmites sp., Vermiculariopsiella dichapetali on leaves of Melaleuca sp. and Eucalyptus regnans, and Xyladictyochaetalusitanica on leaf litter of Eucalyptus sp. (Australia); Camarosporidiella mackenziei on twigs of Caragana sp. (Finland); Cyclothyriella rubronotata on twigs of Ailanthus altissima, Rhinocladiella quercus on Sorbus aucuparia branches (Germany); Cytospora viticola on stems of Vitis vinifera (Hungary); Echinocatena arthrinioides on leaves of Acacia crassicarpa (Malaysia); Varicosporellopsis aquatilis from garden soil (Netherlands); Pestalotiopsis hollandica on needles of Cupressus sempervirens (Spain), Pseudocamarosporiumafricanum on twigs of Erica sp. (South Africa), Pseudocamarosporium brabeji on branch of Platanus sp. (Switzerland); Neocucurbitaria cava on leaves of Quercus ilex (UK); Chaetosphaeriamyriocarpaon decaying wood of Carpinus betulus,Haplograhium delicatum on decaying Carpinus betulus wood (Ukraine). Epitypes are designated for: Elsinoë mimosae on leaves of Mimosa diplotricha (Brazil), Neohendersonia kickxii on Fagus sylvatica twig bark (Italy), Caliciopsis maxima on fronds of Niphidium crassifolium (Brazil), Dictyochaeta septata on leaves of Eucalyptus grandis ×urophylla (Chile), and Microdochium musae on leaves of Musa sp. (Malaysia)

Integrative Effect of Carvedilol and Aerobic Exercise Training Therapies on Improving Cardiac Contractility and Remodeling in Heart Failure Mice

The use of b-blockers is mandatory for counteracting heart failure (HF)-induced chronic sympathetic hyperactivity, cardiac dysfunction and remodeling. Importantly, aerobic exercise training, an efficient nonpharmacological therapy to HF, also counteracts sympathetic hyperactivity in HF and improves exercise tolerance and cardiac contractility; the latter associated with changes in cardiac Ca2+ handling. This study was undertaken to test whether combined b-blocker and aerobic exercise training would integrate the beneficial effects of isolated therapies on cardiac structure, contractility and cardiomyocyte Ca2+ handling in a genetic model of sympathetic hyperactivity-induced HF (alpha(2A)/alpha 2C(-)adrenergic receptor knockout mice, KO). We used a cohort of 5-7 mo male wild-type (WT) and congenic mice (KO) with C57Bl6/J genetic background randomly assigned into 5 groups: control (WT), saline-treated KO (KOS), exercise trained KO (KOT), carvedilol-treated KO (KOC) and, combined carvedilol-treated and exercise-trained KO (KOCT). Isolated and combined therapies reduced mortality compared with KOS mice. Both KOT and KOCT groups had increased exercise tolerance, while groups receiving carvedilol had increased left ventricular fractional shortening and reduced cardiac collagen volume fraction compared with KOS group. Cellular data confirmed that cardiomyocytes from KOS mice displayed abnormal Ca2+ handling. KOT group had increased intracellular peak of Ca2+ transient and reduced diastolic Ca2+ decay compared with KOS group, while KOC had increased Ca2+ decay compared with KOS group. Notably, combined therapies re-established cardiomyocyte Ca2+ transient paralleled by increased SERCA2 expression and SERCA2: PLN ratio toward WT levels. Aerobic exercise trained increased the phosphorylation of PLN at Ser16 and Thr17 residues in both KOT and KOCT groups, but carvedilol treatment reduced lipid peroxidation in KOC and KOCT groups compared with KOS group. the present findings provide evidence that the combination of carvedilol and aerobic exercise training therapies lead to a better integrative outcome than carvedilol or exercise training used in isolation.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Fundação de Amparo à Pesquisa do Estado de Minas Gerais (FAPEMIG)Conselho Nacional de Pesquisa e DesenvolvimentoConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Univ São Paulo, Sch Phys Educ & Sport, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Biosci, Santos, BrazilDept Circulat & Med Imaging, Trondheim, NorwayKG Jebsen Ctr Exercise Med, Trondheim, NorwayUniv Fed Minas Gerais, Dept Physiol & Biophys, Belo Horizonte, MG, BrazilUniv São Paulo, Heart Inst InCor, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Biosci, Santos, BrazilFAPESP: FAPESP:2010/50048-1FAPESP: 06/56123-0CNPq: 302201/2011-4Web of Scienc

Hierarchical and stage-specific regulation of murine cardiomyocyte maturation by serum response factor

After birth, cardiomyocytes (CM) acquire numerous adaptations in order to efficiently pump blood throughout an animal’s lifespan. How this maturation process is regulated and coordinated is poorly understood. Here, we perform a CRISPR/Cas9 screen in mice and identify serum response factor (SRF) as a key regulator of CM maturation. Mosaic SRF depletion in neonatal CMs disrupts many aspects of their maturation, including sarcomere expansion, mitochondrial biogenesis, transverse-tubule formation, and cellular hypertrophy. Maintenance of maturity in adult CMs is less dependent on SRF. This stage-specific activity is associated with developmentally regulated SRF chromatin occupancy and transcriptional regulation. SRF directly activates genes that regulate sarcomere assembly and mitochondrial dynamics. Perturbation of sarcomere assembly but not mitochondrial dynamics recapitulates SRF knockout phenotypes. SRF overexpression also perturbs CM maturation. Together, these data indicate that carefully balanced SRF activity is essential to promote CM maturation through a hierarchy of cellular processes orchestrated by sarcomere assembly

An Analysis of the Myocardial Transcriptome in a Mouse Model of Cardiac Dysfunction with Decreased Cholinergic Neurotransmission

Autonomic dysfunction is observed in many cardiovascular diseases and contributes to cardiac remodeling and heart disease. We previously reported that a decrease in the expression levels of the vesicular acetylcholine transporter (VAChT) in genetically-modified homozygous mice (VAChT KDHOM) leads to decreased cholinergic tone, autonomic imbalance and a phenotype resembling cardiac dysfunction. In order to further understand the molecular changes resulting from chronic long-term decrease in parasympathetic tone, we undertook a transcriptome-based, microarray-driven approach to analyze gene expression changes in ventricular tissue from VAChT KDHOM mice. We demonstrate that a decrease in cholinergic tone is associated with alterations in gene expression in mutant hearts, which might contribute to increased ROS levels observed in these cardiomyocytes. In contrast, in another model of cardiac remodeling and autonomic imbalance, induced through chronic isoproterenol treatment to increase sympathetic drive, these genes did not appear to be altered in a pattern similar to that observed in VAChT KDHOM hearts. These data suggest the importance of maintaining a fine balance between the two branches of the autonomic nervous system and the significance of absolute levels of cholinergic tone in proper cardiac function

FKBP12.6 Deficiency and Defective Calcium Release Channel (Ryanodine Receptor) Function Linked to Exercise-Induced Sudden Cardiac Death

AbstractArrhythmias, a common cause of sudden cardiac death, can occur in structurally normal hearts, although the mechanism is not known. In cardiac muscle, the ryanodine receptor (RyR2) on the sarcoplasmic reticulum releases the calcium required for muscle contraction. The FK506 binding protein (FKBP12.6) stabilizes RyR2, preventing aberrant activation of the channel during the resting phase of the cardiac cycle. We show that during exercise, RyR2 phosphorylation by cAMP-dependent protein kinase A (PKA) partially dissociates FKBP12.6 from the channel, increasing intracellular Ca2+ release and cardiac contractility. FKBP12.6−/− mice consistently exhibited exercise-induced cardiac ventricular arrhythmias that cause sudden cardiac death. Mutations in RyR2 linked to exercise-induced arrhythmias (in patients with catecholaminergic polymorphic ventricular tachycardia [CPVT]) reduced the affinity of FKBP12.6 for RyR2 and increased single-channel activity under conditions that simulate exercise. These data suggest that “leaky” RyR2 channels can trigger fatal cardiac arrhythmias, providing a possible explanation for CPVT

Hierarchical and stage-specific regulation of murine cardiomyocyte maturation by serum response factor

After birth, cardiomyocytes (CM) acquire numerous adaptations in order to efficiently pump blood throughout an animal’s lifespan. How this maturation process is regulated and coordinated is poorly understood. Here, we perform a CRISPR/Cas9 screen in mice and identify serum response factor (SRF) as a key regulator of CM maturation. Mosaic SRF depletion in neonatal CMs disrupts many aspects of their maturation, including sarcomere expansion, mitochondrial biogenesis, transverse-tubule formation, and cellular hypertrophy. Maintenance of maturity in adult CMs is less dependent on SRF. This stage-specific activity is associated with developmentally regulated SRF chromatin occupancy and transcriptional regulation. SRF directly activates genes that regulate sarcomere assembly and mitochondrial dynamics. Perturbation of sarcomere assembly but not mitochondrial dynamics recapitulates SRF knockout phenotypes. SRF overexpression also perturbs CM maturation. Together, these data indicate that carefully balanced SRF activity is essential to promote CM maturation through a hierarchy of cellular processes orchestrated by sarcomere assembly

Abnormalities of calcium metabolism and myocardial contractility depression in the failing heart

Heart failure (HF) is characterized by molecular and cellular defects which jointly contribute to decreased cardiac pump function. During the development of the initial cardiac damage which leads to HF, adaptive responses activate physiological countermeasures to overcome depressed cardiac function and to maintain blood supply to vital organs in demand of nutrients. However, during the chronic course of most HF syndromes, these compensatory mechanisms are sustained beyond months and contribute to progressive maladaptive remodeling of the heart which is associated with a worse outcome. Of pathophysiological significance are mechanisms which directly control cardiac contractile function including ion- and receptor-mediated intracellular signaling pathways. Importantly, signaling cascades of stress adaptation such as intracellular calcium (Ca2+) and 3′-5′-cyclic adenosine monophosphate (cAMP) become dysregulated in HF directly contributing to adverse cardiac remodeling and depression of systolic and diastolic function. Here, we provide an update about Ca2+ and cAMP dependent signaling changes in HF, how these changes affect cardiac function, and novel therapeutic strategies which directly address the signaling defects

Novel fungi from an ancient niche: cercosporoid and related sexual morphs on ferns

The fern flora of the world (Pteridophyta) has direct evolutionary links with the earliest vascular plants that appeared in the late Devonian. Knowing the mycobiota associated to this group of plants is critical for a full understanding of the Fungi. Nevertheless, perhaps because of the minor economic significance of ferns, this niche remains relatively neglected by mycologists. Cercosporoid fungi represent a large assemblage of fungi belonging to the Mycosphaerellaceae and Teratosphaeriaceae (Ascomycota) having cercospora-like asexual morphs. They are well-known pathogens of many important crops, occurring on a wide host range. Here, the results of a taxonomic study of cercosporoid fungi collected on ferns in Brazil are presented. Specimens were obtained from most Brazilian regions and collected over a 7-yr period (2009–2015). Forty-three isolates of cercosporoid and mycosphaerellalike species, collected from 18 host species, representing 201 localities, were studied. This resulted in a total of 21 frond-spotting taxa, which were identified based on morphology, ecology and sequence data of five genomic loci (actin, calmodulin, ITS, LSU and partial translation elongation factor 1-α). One novel genus (Clypeosphaerella) and 15 novel species (Cercospora samambaiae, Clypeosphaerella sticheri, Neoceratosperma alsophilae, N. cyatheae, Paramycosphaerella blechni, Pa. cyatheae, Pa. dicranopteridis-flexuosae, Pa. sticheri, Phaeophleospora pteridivora, Pseudocercospora brackenicola, Ps. paranaensis, Ps. serpocaulonicola, Ps. trichogena, Xenomycosphaerella diplazii and Zasmidium cyatheae) are introduced. Furthermore, 11 new combinations (Clypeosphaerella quasiparkii, Neoceratosperma yunnanensis, Paramycosphaerella aerohyalinosporum, Pa. dicranopteridis, Pa. gleicheniae, Pa. irregularis, Pa. madeirensis, Pa. nabiacense, Pa. parkii, Pa. pseudomarksii and Pa. vietnamensis) are proposed. Finally, nine new host associations are recorded for the following known fungal species: Cercospora coniogrammes, Cercospora sp. Q, Ps. abacopteridicola, Ps. lygodiicola and Ps. thelypteridis