Cambrian Series 3 lithistid sponge–microbial reefs in Shandong Province,North China: reef development after the disappearance of archaeocyaths

The Cambrian Series 3 Zhangxia Formation in Shandong Province, North China, includes small‐scale lithistid sponge–microbial reefs. The lithistid sponges grew on oolitic and bioclastic sediments, which were stabilized by microbial activities. The relative abundances of microbial components (e.g. calcimicrobe Epiphyton and stromatolites) vary among the reefs. However, the microbial components commonly encrusted or bound the lithistid sponges, formed remarkable encrustations on the surfaces of the sponges. Epiphyton especially grew upward and downward. The lithistid sponges thus provided substrates for the attachment and development of microbes, and the microbes played essential roles as consolidators, by encrusting reef‐building sponges. Additionally, the lithistid sponges were prone to degradation via microbial activities and diagenetic processes, and were thus preserved as micritic bodies, showing faint spicular networks or abundant spicules. Such low preservation potential within the reef environment obscured the presence of the sponges and their widespread contribution as reef‐building organisms during the Cambrian. During the prolonged interval after the demise of archaeocyaths, purely microbial reefs, such as stromatolites and thrombolites have been considered to be the principal reef builders, in association with rare lithistid sponge–microbial associations. However, recent findings, including those from Shandong Province and Korea, suggest that the lithistid sponge‐bearing reefs were more extensive during the Epoch 3 to the Furongian than previously thought. These lithistid sponge–microbial reefs were precursors of the sponge–microbial reefs that dominated worldwide in the Early Ordovician.     

Shati/Nat8l Overexpression Improves Cognitive Decline by Upregulating Neuronal Trophic Factor in Alzheimer’s Disease Model Mice

Neurochemical Research - Alzheimer’s disease (AD) is a type of dementia characterized by the deposition of amyloid β, a causative protein of AD, in the brain. Shati/Nat8l, identified as...     

NISES-AnPe-428 cell line derived from the Chinese oak silkworm Antheraea pernyi is permissive for multiple nucleopolyhedrovirus species from insects of four different families

Cytotechnology - The cell line NISES-AnPe-428 (AnPe), derived from the Chinese oak silkworm Antheraea pernyi, was characterized for its permissiveness and productivity for six different...     

Spectroscopic studies of interactions of chondroitin sulfates with cisplatin

Complexation of cisplatin (CDDP) and chondroitin sulfate A (CSA) or C (CSC) has been reported to reduce the nephrotoxicity of CDDP. However the mechanism of interaction between CDDP and CSA or CSC was not known. In this study, spectroscopic analyses including NMR were carried out to examine the complexation interactions of CSA and CSC with CDDP. The time-dependent changes in the UV spectra indicate that CSA and CSC effectively complexes with CDDP in aqueous solution and that the reaction occurs subsequent to the hydrolysis of CDDP. The time-dependent change results measured by capillary electrophoresis showed that complexation of chondroitin sulfate (CS) followed first-order reaction kinetics and that the rate of CDDP hydrolysis in the complexation for both CSA and CSC was the same. These results suggested that the mechanism of complexation was a two-step process with monoaqua formation proved to be the first step, which was also the reaction rate controlling step. Moreover, NMR data suggested that the carboxylic and sulfate groups of CS played an important role in its interaction with CDDP.     

Predation risk suppresses the positive feedback between size structure and cannibalism

1.?Cannibalism can play a prominent role in the structuring and dynamics of ecological communities. Previous studies have emphasized the importance of size structure and density of cannibalistic species in shaping short- and long-term cannibalism dynamics, but our understanding of how predators influence cannibalism dynamics is limited. This is despite widespread evidence that many prey species exhibit behavioural and morphological adaptations in response to predation risk. 2.?This study examined how the presence and absence of predation risk from larval dragonflies Aeshna nigroflava affected cannibalism dynamics in its prey larval salamanders Hynobius retardatus. 3.?We found that feedback dynamics between size structure and cannibalism depended on whether dragonfly predation risk was present. In the absence of dragonfly risk cues, a positive feedback between salamander size structure and cannibalism through time occurred because most of the replicates in this treatment contained at least one salamander larvae having an enlarged gape (i.e. cannibal). In contrast, this feedback and the emergence of cannibalism were rarely observed in the presence of the dragonfly risk cues. Once salamander size divergence occurred, experimental reversals of the presence or absence of dragonfly risk cues did not alter existing cannibalism dynamics as the experiment progressed. Thus, the effects of risk on the mechanisms driving cannibalism dynamics likely operated during the early developmental period of the salamander larvae. 4.?The effects of dragonfly predation risk on behavioural aspects of cannibalistic interactions among hatchlings may prohibit the initiation of dynamics between size structure and cannibalism. Our predation trials clearly showed that encounter rates among hatchlings and biting and ingestion rates of prospective prey by prospective cannibals were significantly lower in the presence vs. absence of dragonfly predation risk even though the size asymmetry between cannibals and victims was similar in both risk treatments. These results suggest that dragonfly risk cues first suppress cannibalism among hatchlings and then prevent size variation from increasing through time. 5.?We suggest that the positive feedback dynamics between size structure and cannibalism and their modification by predation risk may also operate in other systems to shape the population dynamics of cannibalistic prey species as well as overall community dynamics.     

Characterization of endogenous substrates for novel-type protein kinase C as well as conventional-type protein kinase C in primary cultured mouse epidermal cells

In primary cultured mouse epidermal cells, phorbol 12-myristate 13-acetate (PMA), which activates protein kinase C (PKC), induced changes in the phosphorylation levels of 10 proteins, termed KP-1 to 10, in two-dimensional PAGE. Seven of these proteins were phosphorylated and three were dephosphorylated. Similar changes were induced by other PKC activators, but not by inactive phorbol ester. Among these substrate proteins, phosphorylation of three proteins, i.e. KP-1 (pI 4.7/23,000 M_r), KP-2 (pI 4.7/20,700 M_r) and KP-10 (pI 4.7/25,000 M_r was markedly enhanced by PMA and inhibited by a potent PKC inhibitor staurosporine. In vitro phosphorylation studies and phosphoamino acid analysis, using these proteins as substrate and PKC preparations obtained from epidermal cell lysate, revealed that KP-1 and -2 were directly phosphorylated by Ca²⁺-, phospholipid-dependent protein kinase (conventional-type PKC; cPKC), but not by Ca²⁺-independent, phospholipid-dependent protein kinase (novel-type PKC; nPKC). On the other hand, KP-10 was mainly phosphorylated by nPKC in intact epidermal cells. These results indicate that cPKC and nPKC in epidermal cells have different substrate specificity for endogenous proteins and may induce different signal transduction.     

Identification of genes affecting the toxicity of anti-cancer drug bortezomib by genome-wide screening in S. pombe

Bortezomib/PS-341/Velcade, a proteasome inhibitor, is widely used to treat multiple myeloma. While several mechanisms of the cytotoxicity of the drug were proposed, the actual mechanism remains elusive. We aimed to identify genes affecting the cytotoxicity of Bortezomib in the fission yeast S. pombe as the drug inhibits this organism's cell division cycle like proteasome mutants. Among the 2815 genes screened (covering 56% of total ORFs), 19 genes, whose deletions induce strong synthetic lethality with Bortezomib, were identified. The products of the 19 genes included four ubiquitin enzymes and one nuclear proteasome factor, and 13 of them are conserved in humans. Our results will provide useful information for understanding the actions of Bortezomib within cells.