Ocean province classification using ocean colour data: observing biological signatures of variations in physical dynamics

We have used satellite colour data to classify ocean environments for monitoring interannual changes in the ocean. The unsupervised classification method is based on our observation that the frequency distributions of Coastal Zone Color Scanner (CZCS) annual pigment means and standard deviations are nonuniform and contain distinct clusters. The frequency distributions are used to objectively determine ocean areas with similar pigment statistical characteristics. A major separation between high variance, high pigment and lower variance, lower pigment waters is observed in terms of global ocean area. The ocean areas determined with our method reflect different bio‐logical responses to variations in ocean physical dynamics. Pigment means and variances around the Joint Global Ocean Flux Study (JGOFS) Time Series stations are used as fiducial characteristics. Hawaii Ocean Time‐series (HOT) station is associated with the low‐variance portion of the global annual pigment distribution characteristic of the central gyres, but shows slightly higher mean and variance than the minima in the central Pacific gyre. The Bermuda Atlantic Time Series (BATS) pigment associations comprise a transitional region between the gyres and high‐variance pigment areas, and circumscribe the HOT pigment associations. Together, these associations encompass 23% (HOT‐like) and 48% (BATS‐like) of the Northern Hemisphere open ocean. The Pacific regions delineated by the JGOFS station pigment‐based patterns are similar to distributions described historically for Pacific zooplankton communities. Interannual variation for the northern hemisphere gyre area is on the order of by 10% for the 11/78–10/81 period.     

Kinetics of O2 uptake, leg blood flow, and muscle deoxygenation are slowed in the upper compared with lower region of the moderate-intensity exercise domain.

Six male subjects [23 yr (SD 4)] performed repetitions (6-8) of two-legged, moderate-intensity, knee-extension exercise during two separate protocols that included step transitions from 3 W to 90% estimated lactate threshold (thetaL) performed as a single step (S3) and in two equal steps (S1, 3 W to approximately 45% thetaL; S2, approximately 45% thetaL to approximately 90% thetaL). The time constants (tau) of pulmonary oxygen uptake (Vo2), leg blood flow (LBF), heart rate (HR), and muscle deoxygenation (HHb) were greater (P < 0.05) in S2 (tauVo2, approximately 52 s; tauLBF, approximately 39 s; tauHR, approximately 42 s; tauHHb, approximately 33 s) compared with S1 (tauVo2, approximately 24 s; tauLBF, approximately 21 s; tauHR, approximately 21 s; tauHHb, approximately 16 s), while the delay before an increase in HHb was reduced (P < 0.05) in S2 (approximately 14 s) compared with S1 (approximately 20 s). The Vo2 and HHb amplitudes were greater (P < 0.05) in S2 compared with S1, whereas the LBF amplitude was similar in S2 and S1. Thus the slowed Vo2 response in S2 compared with S1 is consistent with a mechanism whereby Vo2 kinetics is limited, in part, by a slowed adaptation of blood flow and/or O2 transport when exercise was initiated from a baseline of moderate-intensity exercise.     

Timescales of genetic and epigenetic inheritance

According to classical evolutionary theory, phenotypic variation originates from random mutations that are independent of selective pressure. However, recent findings suggest that organisms have evolved mechanisms to influence the timing or genomic location of heritable variability. Hypervariable contingency loci and epigenetic switches increase the variability of specific phenotypes; error-prone DNA replicases produce bursts of variability in times of stress. Interestingly, these mechanisms seem to tune the variability of a given phenotype to match the variability of the acting selective pressure. Although these observations do not undermine Darwin's theory, they suggest that selection and variability are less independent than once thought.     

Microbial reductive dechlorination of aroclor 1260 in Baltimore harbor sediment microcosms is catalyzed by three phylotypes within the phylum Chloroflexi

The specific dechlorination pathways for Aroclor 1260 were determined in Baltimore Harbor sediment microcosms developed with the 11 most predominant congeners from this commercial mixture and their resulting dechlorination intermediates. Most of the polychlorinated biphenyl (PCB) congeners were dechlorinated in the meta position, and the major products were tetrachlorobiphenyls with unflanked chlorines. Using PCR primers specific for the 16S rRNA genes of known PCB-dehalogenating bacteria, we detected three phylotypes within the microbial community that had the capability to dechlorinate PCB congeners present in Aroclor 1260 and identified their selective activities. Phylotype DEH10, which has a high level of sequence identity to Dehalococcoides spp., removed the double-flanked chlorine in 234-substituted congeners and exhibited a preference for para-flanked meta-chlorines when no double-flanked chlorines were available. Phylotype SF1 had similarity to the o-17/DF-1 group of PCB-dechlorinating bacteria. Phylotype SF1 dechlorinated all of the 2345-substituted congeners, mostly in the double-flanked meta position and 2356-, 236-, and 235-substituted congeners in the ortho-flanked meta position, with a few exceptions. A phylotype with 100% sequence identity to PCB-dechlorinating bacterium o-17 was responsible for an ortho and a double-flanked meta dechlorination reaction. Most of the dechlorination pathways supported the growth of all three phylotypes based on competitive PCR enumeration assays, which indicates that PCB-impacted environments have the potential to sustain populations of these PCB-dechlorinating microorganisms. The results demonstrate that the variation in dechlorination patterns of congener mixtures typically observed at different PCB impacted sites can potentially be mediated by the synergistic activities of relatively few dechlorinating species.     

Characterization of airborne molds, endotoxins, and glucans in homes in New Orleans after Hurricanes Katrina and Rita

In August and September 2005, Hurricanes Katrina and Rita caused breeches in the New Orleans, LA, levee system, resulting in catastrophic flooding. The city remained flooded for several weeks, leading to extraordinary mold growth in homes. To characterize the potential risks of mold exposures, we measured airborne molds and markers of molds and bacteria in New Orleans area homes. In October 2005, we collected air samples from 5 mildly water-damaged houses, 15 moderately to heavily water-damaged houses, and 11 outdoor locations. The air filters were analyzed for culturable fungi, spores, (1-->3,1-->6)-beta-D-glucans, and endotoxins. Culturable fungi were significantly higher in the moderately/heavily water-damaged houses (geometric mean=67,000 CFU/m3) than in the mildly water-damaged houses (geometric mean=3,700 CFU/m3) (P=0.02). The predominant molds found were Aspergillus niger, Penicillium spp., Trichoderma, and Paecilomyces. The indoor and outdoor geometric means for endotoxins were 22.3 endotoxin units (EU)/m3 and 10.5 EU/m3, respectively, and for (1-->3,1-->6)-beta-D-glucans were 1.7 microg/m3 and 0.9 microg/m3, respectively. In the moderately/heavily water-damaged houses, the geometric means were 31.3 EU/m3 for endotoxins and 1.8 microg/m3 for (1-->3,1-->6)-beta-D-glucans. Molds, endotoxins, and fungal glucans were detected in the environment after Hurricanes Katrina and Rita in New Orleans at concentrations that have been associated with health effects. The species and concentrations were different from those previously reported for non-water-damaged buildings in the southeastern United States.     

Biodegradation of bis(2-chloroethyl) ether by Xanthobacter sp. strain ENV481

Degradation of bis(2-chloroethyl) ether (BCEE) was observed to occur in two bacterial strains. Strain ENV481, a Xanthobacter sp. strain, was isolated by enrichment culturing of samples from a Superfund site located in the northeastern United States. The strain was able to grow on BCEE or 2-chloroethylethyl ether as the sole source of carbon and energy. BCEE degradation in strain ENV481 was facilitated by sequential dehalogenation reactions resulting in the formation of 2-(2-chloroethoxy)ethanol and diethylene glycol (DEG), respectively. 2-Hydroxyethoxyacetic acid was detected as a product of DEG catabolism by the strain. Degradation of BCEE by strain ENV481 was independent of oxygen, and the strain was not able to grow on a mixture of benzene, ethylbenzene, toluene, and xylenes, other prevalent contaminants at the site. Another bacterial isolate, Pseudonocardia sp. strain ENV478 (S. Vainberg et al., Appl. Environ. Microbiol. 72:5218-5224, 2006), degraded BCEE after growth on tetrahydrofuran or propane but was not able to grow on BCEE as a sole carbon source. BCEE degradation by strain ENV478 appeared to be facilitated by a monooxygenase-mediated O-dealkylation mechanism, and it resulted in the accumulation of 2-chloroacetic acid that was not readily degraded by the strain.     

Physiological roles of STIM1 and Orai1 homologs and CRAC channels in the genetic model organism Caenorhabditis elegans

The nematode Caenorhabditis elegans provides numerous experimental advantages for developing an integrative molecular understanding of physiological processes and has proven to be a valuable model for characterizing Ca(2+) signaling mechanisms. This review will focus on the role of Ca(2+) release activated Ca(2+) (CRAC) channel activity in function of the worm gonad and intestine. Inositol 1,4,5-trisphosphate (IP(3))-dependent oscillatory Ca(2+) signaling regulates contractile activity of the gonad and rhythmic posterior body wall muscle contraction (pBoc) required for ovulation and defecation, respectively. The C. elegans genome contains a single homolog of both STIM1 and Orai1, proteins required for CRAC channel function in mammalian and Drosophila cells. C. elegans STIM-1 and ORAI-1 are coexpressed in the worm gonad and intestine and give rise to robust CRAC channel activity when coexpressed in HEK293 cells. STIM-1 or ORAI-1 knockdown causes complete sterility demonstrating that the genes are essential components of gonad Ca(2+) signaling. Knockdown of either protein dramatically inhibits intestinal cell CRAC channel activity, but surprisingly has no effect on pBoc, intestinal Ca(2+) oscillations or intestinal ER Ca(2+) store homeostasis. CRAC channels thus do not play obligate roles in all IP(3)-dependent signaling processes in C. elegans. Instead, we suggest that CRAC channels carry out highly specialized and cell specific signaling roles and that they may function as a failsafe mechanism to prevent Ca(2+) store depletion under pathophysiological and stress conditions.