Variations in Temperature Sensitivity (Q10) of CH4 Emission from a Subtropical Estuarine Marsh in Southeast China

Understanding the functional relationship between greenhouse gas fluxes and environmental variables is crucial for predicting the impacts of wetlands on future climate change in response to various perturbations. We examined the relationships between methane (CH₄) emission and temperature in two marsh stands dominated by the Phragmites australis and Cyperus malaccensis, respectively, in a subtropical estuarine wetland in southeast China based on three years of measurement data (2007–2009). We found that the Q₁₀ coefficient of CH₄ emission to soil temperature (Q_s10) from the two marsh stands varied slightly over the three years (P > 0.05), with a mean value of 3.38 ± 0.46 and 3.89 ± 0.41 for the P. australis and C. malaccensis stands, respectively. On the other hand, the three-year mean Q_a10 values (Q₁₀ coefficients of CH₄ emission to air temperature) were 3.39 ± 0.59 and 4.68 ± 1.10 for the P. australis and C. malaccensis stands, respectively, with a significantly higher Q_a10 value for the C. malaccensis stand in 2008 (P < 0.05). The seasonal variations of Q₁₀ (Q_s10 and Q_a10) differed among years, with generally higher values in the cold months than those in the warm months in 2007 and 2009. We found that the Q_s10 values of both stands were negatively correlated with soil conductivity, but did not obtain any conclusive results about the difference in Q₁₀ of CH₄ emission between the two tidal stages (before flooding and after ebbing). There were no significant differences in both Q_s10 and Q_a10 values of CH₄ emission between the P. australis stand and the C. malaccensis stands (P > 0.05). Our results show that the Q₁₀ values of CH₄ emission in this estuarine marsh are highly variable across space and time. Given that the overall CH₄ flux is governed by a suite of environmental factors, the Q₁₀ values derived from field measurements should only be considered as a semi-empirical parameter for simulating CH₄ emissions.     

Effects of Adenine Derivatives and Auxin-related Compounds on Mitochondrial Membrane Permeability

Adenine derivatives and auxin-related compounds, 2,4-dichlorophenoxyaceticacid (2,4-D) and 2,3,5-triiodobenzoic acid (TIBA), did not inhibitthe transport systems for succinate or malate into mitochondria.In iso-osmotic KC1 medium, some of these compounds increasedion fluxes moderately. TIBA and 2,4-D inhibited the mitochondrialshrinkage induced by the substrates. In contrast, adenine derivativesinhibited only the shrinkage induced by the substrate whoseoxidation they were able to block specifically. (Received February 18, 1987; Accepted June 29, 1987)     

The Ighmbp2 helicase structure reveals the molecular basis for disease-causing mutations in DMSA1

Mutations in immunoglobulin µ-binding protein 2 (Ighmbp2) cause distal spinal muscular atrophy type 1 (DSMA1), an autosomal recessive disease that is clinically characterized by distal limb weakness and respiratory distress. However, despite extensive studies, the mechanism of disease-causing mutations remains elusive. Here we report the crystal structures of the Ighmbp2 helicase core with and without bound RNA. The structures show that the overall fold of Ighmbp2 is very similar to that of Upf1, a key helicase involved in nonsense-mediated mRNA decay. Similar to Upf1, domains 1B and 1C of Ighmbp2 undergo large conformational changes in response to RNA binding, rotating 30° and 10°, respectively. The RNA binding and ATPase activities of Ighmbp2 are further enhanced by the R3H domain, located just downstream of the helicase core. Mapping of the pathogenic mutations of DSMA1 onto the helicase core structure provides a molecular basis for understanding the disease-causing consequences of Ighmbp2 mutations.     

Detection of a Novel Unglycosylated Form of Hepatitis C Virus E2 Envelope Protein That Is Located in the Cytosol and Interacts with PKR

The hepatitis C virus (HCV) envelope protein E2 has been shown to accumulate in the lumen of the endoplasmic reticulum (ER) as a properly folded glycoprotein as well as large aggregates of misfolded proteins. In the present study, we have identified an additional unglycosylated species, with an apparent molecular mass of 38 kDa (E2-p38). In contrast to the glycosylated E2, E2-p38 is significantly less stable and is degraded through the proteasome pathway. Correspondingly, E2-p38 is found to be ubiquitinated. E2-p38 is localized mostly in the cytosol, in contrast to the glycosylated form, which is exclusively membrane associated. Alpha interferon (IFN-alpha) treatment or overexpression of the double-stranded RNA-activated protein kinase (PKR) significantly increased the stability of E2-p38, consistent with a previous report (D. R. Taylor, S. T. Shi, P. R. Romano, G. N. Barber, and M. M. Lai, Science 285:107-110, 1999) that E2 interacts with PKR and inhibits its kinase activity. Direct interaction between PKR and E2-p38, but not the glycosylated form of E2, was also observed. These results show that E2-p38 is the form of E2 that interacts with PKR in the cytosol and may contribute to the resistance of HCV to IFN-alpha. Thus, an ER protein can exist in the cytosol as an unglycosylated species and impair cellular functions.     

Alternative splice isoforms of small conductance calcium-activated SK2 channels differ in molecular interactions and surface levels

Small conductance Ca²⁺-sensitive potassium (SK2) channels are voltage-independent, Ca²⁺-activated ion channels that conduct potassium cations and thereby modulate the intrinsic excitability and synaptic transmission of neurons and sensory hair cells. In the cochlea, SK2 channels are functionally coupled to the highly Ca²⁺ permeant α9/10-nicotinic acetylcholine receptors (nAChRs) at olivocochlear postsynaptic sites. SK2 activation leads to outer hair cell hyperpolarization and frequency-selective suppression of afferent sound transmission. These inhibitory responses are essential for normal regulation of sound sensitivity, frequency selectivity, and suppression of background noise. However, little is known about the molecular interactions of these key functional channels. Here we show that SK2 channels co-precipitate with α9/10-nAChRs and with the actin-binding protein α-actinin-1. SK2 alternative splicing, resulting in a 3 amino acid insertion in the intracellular 3′ terminus, modulates these interactions. Further, relative abundance of the SK2 splice variants changes during developmental stages of synapse maturation in both the avian cochlea and the mammalian forebrain. Using heterologous cell expression to separately study the 2 distinct isoforms, we show that the variants differ in protein interactions and surface expression levels, and that Ca²⁺ and Ca²⁺-bound calmodulin differentially regulate their protein interactions. Our findings suggest that the SK2 isoforms may be distinctly modulated by activity-induced Ca²⁺ influx. Alternative splicing of SK2 may serve as a novel mechanism to differentially regulate the maturation and function of olivocochlear and neuronal synapses.