Three major mesoplanktonic communities resolved by in situ imaging in the upper 500 m of the global ocean

Aim

The distribution of mesoplankton communities has been poorly studied at global scale, especially from in situ instruments. This study aims to (1) describe the global distribution of mesoplankton communities in relation to their environment and (2) assess the ability of various environmental-based ocean regionalizations to explain the distribution of these communities.

Location

Global ocean, 0–500 m depth.

Time Period

2008–2019.

Major Taxa Studied

Twenty-eight groups of large mesoplanktonic and macroplanktonic organisms, covering Metazoa, Rhizaria and Cyanobacteria.

Methods

From a global data set of 2500 vertical profiles making use of the Underwater Vision Profiler 5 (UVP5), an in situ imaging instrument, we studied the global distribution of large (>600 μm) mesoplanktonic organisms. Among the 6.8 million imaged objects, 330,000 were large zooplanktonic organisms and phytoplankton colonies, the rest consisting of marine snow particles. Multivariate ordination (PCA) and clustering were used to describe patterns in community composition, while comparison with existing regionalizations was performed with regression methods (RDA).

Results

Within the observed size range, epipelagic plankton communities were Trichodesmium-enriched in the intertropical Atlantic, Copepoda-enriched at high latitudes and in upwelling areas, and Rhizaria-enriched in oligotrophic areas. In the mesopelagic layer, Copepoda-enriched communities were also found at high latitudes and in the Atlantic Ocean, while Rhizaria-enriched communities prevailed in the Peruvian upwelling system and a few mixed communities were found elsewhere. The comparison between the distribution of these communities and a set of existing regionalizations of the ocean suggested that the structure of plankton communities described above is mostly driven by basin-level environmental conditions.

Main Conclusions

In both layers, three types of plankton communities emerged and seemed to be mostly driven by regional environmental conditions. This work sheds light on the role not only of metazoans, but also of unexpected large protists and cyanobacteria in structuring large mesoplankton communities.     

Respiration and carbohydrate energy metabolism of the lung-dwelling parasite Rhabdias bufonis (Nematoda: Rhabdiasoidea)

An investigation of the carbohydrate energy metabolism of Rhabdias bufonis, the lung-dwelling nematode parasite of the African toad, Bufo regularis, indicates that the nematode stores very little glycogen (0.137 +/- 0.003% on a fresh weight basis) but does utilize oxygen in vitro. The intracellular distribution and high levels of activity observed for the enzymes phosphoenolpyruvate carboxykinase, pyruvate kinase, lactate dehydrogenase, malate dehydrogenase, malic enzyme and fumarate reductase suggest two alternative pathways of carbohydrate energy metabolism.     

What is hidden in the pannexin treasure trove: the sneak peek and the guesswork

Connexins had been considered to be the only class of the vertebrate proteins capable of gap junction formation; however, new candidates for this function with no homology to connexins, termed pannexins were discovered. So far three pannexins were described in rodent and human genomes: Panx1, Panx2 and Panx3. Expressions of pannexins can be detected in numerous brain structures, and now found both in neuronal and glial cells. Hypothetical roles of pannexins in the nervous system include participating in sensory processing, hippocampal plasticity, synchronization between hippocampus and cortex, and propagation of the calcium waves supported by glial cells, which help maintain and modulate neuronal metabolism. Pannexin also may participate in pathological reactions of the neural cells, including their damage after ischemia and subsequent cell death. Recent study revealed non-gap junction function of Panx1 hemichannels in erythrocytes, where they serve as the conduits for the ATP release in response to the osmotic stress. High-throughput studies produced some evidences of the pannexin involvement in the process of tumorigenesis. According to brain cancer gene expression database REMBRANDT, PANX2 expression levels can predict post diagnosis survival for patients with glial tumors. Further investigations are needed to verify or reject hypotheses listed.     

Interaction of human HelQ with DNA polymerase delta halts DNA synthesis and stimulates DNA single-strand annealing

DNA strand breaks are repaired by DNA synthesis from an exposed DNA end paired with a homologous DNA template. DNA polymerase delta (Pol δ) catalyses DNA synthesis in multiple eukaryotic DNA break repair pathways but triggers genome instability unless its activity is restrained. We show that human HelQ halts DNA synthesis by isolated Pol δ and Pol δ-PCNA-RPA holoenzyme. Using novel HelQ mutant proteins we identify that inhibition of Pol δ is independent of DNA binding, and maps to a 70 amino acid intrinsically disordered region of HelQ. Pol δ and its POLD3 subunit robustly stimulated DNA single-strand annealing by HelQ, and POLD3 and HelQ interact physically via the intrinsically disordered HelQ region. This data, and inability of HelQ to inhibit DNA synthesis by the POLD1 catalytic subunit of Pol δ, reveal a mechanism for limiting DNA synthesis and promoting DNA strand annealing during human DNA break repair, which centres on POLD3.     

CENP-A is essential for cardiac progenitor cell proliferation

Centromere protein A (CENP-A) is a homolog of histone H3 that epigenetically marks the heterochromatin of chromosomes. CENP-A is a critical component of the cell cycle machinery that is necessary for proper assembly of the mitotic spindle. However, the role of CENP-A in the heart and cardiac progenitor cells (CPCs) has not been previously studied. This study shows that CENP-A is expressed in CPCs and declines with age. Silencing CENP-A results in a decreased CPC growth rate, reduced cell number in phase G₂/M of the cell cycle, and increased senescence associated β-galactosidase activity. Lineage commitment is not affected by CENP-A silencing, suggesting that cell cycle arrest induced by loss of CENP-A is a consequence of senescence and not differentiation. CENP-A knockdown does not exacerbate cell death in undifferentiated CPCs, but increases apoptosis upon lineage commitment. Taken together, these results indicate that CPCs maintain relatively high levels of CENP-A early in life, which is necessary for sustaining proliferation, inhibiting senescence, and promoting survival following differentiation of CPCs.     

Differential effects of carboxyfullerene on MPP+/MPTP-induced neurotoxicity

The effects of carboxyfullerene on a well-known neurotoxin, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and its active metabolite 1-methyl-4-phenyl-pyridinium (MPP+) were investigated. In chloral hydrate-anesthetized rats, cytosolic cytochrome c was elevated in the infused substantia nigra 4 h after an intranigral infusion of MPP+. Five days after local application of MPP+, lipid peroxidation (LP) was elevated in the infused substantia nigra. Furthermore, dopamine content and tyrosine hydroxylase (TH)-positive axons were reduced in the ipsilateral striatum. Concomitant intranigral infusion of carboxyfullerene abolished the elevation in cytochrome c and oxidative injuries induced by MPP+. In contrast, systemic application of carboxyfullerene did not prevent neurotoxicity induced by intraperitoneal injection of MPTP. In mice, systemic administration of MPTP induced a dose-dependent depletion in striatal dopamine content. Simultaneous injection of carboxyfullerene (10 mg/kg) actually potentiated MPTP-induced reduction in striatal dopamine content. Furthermore, systemic administration of carboxyfullerene (30 mg/kg) caused death in the MPTP-treated mice. An increase in the striatal MPP+ level and reduction in hepatic P450 level were observed in the carboxyfullerene co-treated mice. These data showed that systemic application of carboxyfullerene appears to potentiate MPTP-induced neurotoxicity while local carboxyfullerene has been suggested as a neuroprotective agent. Furthermore, an increase in striatal MPP+ level may contribute to the potentiation by carboxyfullerene of MPTP-induced neurotoxicity.     

Correction to: Genetic diversity and reproductive ecology of the sage-leaved rockrose,Cistus salviifolius L., in the Swiss Alps

Plant Ecology - Figure 1 has been published incorrectly in the original article. The correct version of Figure 1 is provided in this correction.     

mTOR signaling for biological control and cancer

Mammalian target of rapamycin (mTOR) is a major intersection that connects signals from the extracellular milieu to corresponding changes in intracellular processes. When abnormally regulated, the mTOR signaling pathway is implicated in a wide spectrum of cancers, neurological diseases, and proliferative disorders. Therefore, pharmacological agents that restore the regulatory balance of the mTOR pathway could be beneficial for a great number of diseases. This review summarizes current understanding of mTOR signaling and some unanswered questions in the field. We describe the composition of the mTOR complexes, upstream signals that activate mTOR, and physiological processes that mTOR regulates. We also discuss the role of mTOR and its downstream effectors in cancer, obesity and diabetes, and autism. J. Cell. Physiol. 228: 1658–1664, 2013. © 2013 Wiley Periodicals, Inc.     

Phosphorylation of C-terminal polycystin-2 influences the interaction with PIGEA14: A QCM study based on solid supported membranes

Polycystin-2 (PC2) trafficking has been proposed to be a result of the interaction of PIGEA14 with PC2 as a function of the phosphorylation state of PC2. Here, we investigated the interaction of PIGEA14 with the C-terminal part of polycystin-2 wild type (cPC2wt) and the pseudophosphorylated mutant (cPC2S812D) to first, quantify the binding affinity between cPC2 and PIGEA14 and second, to elucidate the influence of PC2 phosphorylation on PIGEA14 binding. Solid supported membranes composed of octanethiol/1,2-dioleoyl-sn-glycero-3-phosphocholine doped with the receptor lipid DOGS–NTA–Ni were used to attach PIGEA14 to the membrane via its hexahistidine tag. By means of the quartz crystal microbalance technique, binding affinities as well as kinetic constants of the interaction were extracted in a label-free manner by applying the scaled particle theory. The results show that the dissociation constant of cPC2 to PIGEA14 is in the 10 nM regime providing strong evidence of a very specific interaction of cPC2 with PIGEA14. The interaction of cPC2wt is twofold larger than that of cPC2S812D. The moderate higher binding affinity of cPC2wt to PIGEA14 is discussed in light of PC2 trafficking to the plasma membrane.