Phytophthora acaciivora sp. nov. associated with dying Acacia mangium in Vietnam.

Acacia mangium plantations account for more than 50 % of the exotic plantations in Vietnam. A new black butt symptom was discovered in 2012, followed by the wilting sign in Acacia seedlings in Tuyen Quang Province. Isolations recovered two Phytophthora species, the well-known Acacia pathogen P. cinnamomi, and an unknown species. The new species is described here as Phytophthora acaciivora sp. nov. Phylogenetically this species resides in clade 2d and is most closely related to P. frigida. Phytophthora acaciivora is a heterothallic species, oospores are aplerotic and antheridia are amphigynous. It produces predominantly elongated ovoid, semi papillate, persistent sporangia, no hyphal swellings and no chlamydospores. Optimum temperature for the growth is 25-30 °C and the maximum temperature is over 37.5 °C. Studies are underway to determine the impact of this new species on Acacia plantations in Vietnam.

Regulation of cardiomyocyte mechanotransduction by the cardiac cycle.

BACKGROUND: Overloading the left ventricle in systole (pressure overload) is associated with a distinct morphological response compared with overload in diastole (volume overload). METHODS AND RESULTS: We designed a novel computer-controlled experimental system that interfaces biaxially uniform strain with electrical pacing, so that cellular deformation can be imposed during a specified phase of the cardiac cycle. Cardiomyocytes were exposed to strain (4%) during either the first third (systolic phase) or last third (diastolic phase) of the cardiac cycle. Strain imposed during the systolic phase selectively activated p44/42 mitogen-activated protein kinase (MAPK) and MAPK/extracellular signal-regulated protein kinase kinase (MEK1/2, an activator of p44/42 MAPK) compared with strain imposed during the diastolic phase. In contrast, there was no difference in activation of p38 and c-Jun NH(2)-terminal kinases induced by strain imposed during the systolic phase (5.8- and 3.3-fold versus control, n=4) compared with the diastolic phase (5.5- and 3.1-fold). Induction of both brain natriuretic peptide (5.8-fold versus control, P:<0.05, n=3) and tenascin-C (7.0-fold, P:<0.02) mRNA expression by strain imposed during the systolic phase was greater than during the diastolic phase (3.9- and 3.6-fold, respectively). [(3)H]leucine incorporation induced by strain imposed during the systolic phase (4.0-fold versus control) was greater than during the diastolic phase (2.7-fold, P:<0.02, n=4); a selective inhibitor of MEK1/2 inhibited this difference. CONCLUSIONS: Mechanical activation of p44/42 MAPK and MEK1/2, gene expression, and protein synthesis is regulated by the cardiac cycle, suggesting that mechanotransduction at the cellular level may underlie differences between pressure and volume overload of the heart.

Induction of tenascin-C in cardiac myocytes by mechanical deformation. Role of reactive oxygen species.

Mechanical overload may change cardiac structure through angiotensin II-dependent and angiotensin II-independent mechanisms. We investigated the effects of mechanical strain on the gene expression of tenascin-C, a prominent extracellular molecule in actively remodeling tissues, in neonatal rat cardiac myocytes. Mechanical strain induced tenascin-C mRNA (3.9 +/- 0.5-fold, p < 0.01, n = 13) and tenascin-C protein in an amplitude-dependent manner but did not induce secreted protein acidic and rich in cysteine nor fibronectin. RNase protection assay demonstrated that mechanical strain induced all three alternatively spliced isoforms of tenascin-C. An angiotensin II receptor type 1 antagonist inhibited mechanical induction of brain natriuretic peptide but not tenascin-C. Antioxidants such as N-acetyl-L-cysteine, catalase, and 1, 2-dihydroxy-benzene-3,5-disulfonate significantly inhibited induction of tenascin-C. Truncated tenascin-C promoter-reporter assays using dominant negative mutants of IkappaBalpha and IkappaB kinase beta and electrophoretic mobility shift assays indicated that mechanical strain increases tenascin-C gene transcription by activating nuclear factor-kappaB through reactive oxygen species. Our findings demonstrate that mechanical strain induces tenascin-C in cardiac myocytes through a nuclear factor-kappaB-dependent and angiotensin II-independent mechanism. These data also suggest that reactive oxygen species may participate in mechanically induced left ventricular remodeling.

Mechanical strain suppresses inducible nitric-oxide synthase in cardiac myocytes.

We investigated the effects of precisely controlled mechanical strain on nitric-oxide synthase activity in cultured neonatal rat cardiac myocytes. Incubation of cardiac myocytes for 24 h with 4 ng/ml interleukin-1beta and 100 units/ml interferon-gamma stimulated an increase in nitric oxide production, inducible nitric-oxide synthase (iNOS) mRNA, and iNOS protein. Mechanical strain suppressed nitric oxide production, iNOS mRNA, and iNOS protein stimulated by cytokines in an amplitude-dependent manner. Losartan (1 microM), an angiotensin II type 1 receptor antagonist, weakly inhibited the effect of strain, suggesting that paracrine angiotensin II is not the mediator of the strain effect. In addition, cycloheximide (10 microM), a protein synthesis inhibitor, inhibited the effect of strain by 46%. Transforming growth factor-beta (1 ng/ml) suppressed iNOS mRNA expression, but anti-transforming growth factor-beta antibody (30 microg/ml) did not block the effect of strain. In contrast, staurosporine (100 nM; a nonselective protein kinase inhibitor), calphostin C (1 microM; a selective protein kinase C inhibitor), and pretreatment with phorbol 12-myristate 13-acetate abolished the effect of strain. Genistein (100 microM), a tyrosine kinase inhibitor, partially inhibited the effect of strain. Thus, cyclic mechanical deformation suppresses cytokine-induced iNOS expression in cardiac myocytes, and this effect is mediated at least partially via activation of protein kinase C.