Jellyfish menace in estuarine Stake nets operated off Kochi, Kerala

Jellyfish are distributed around the world oceans and estuaries, living from surface to greatest depths. These gelatinous zooplankton, belonging to Phylum Cnidaria, an ancient phylum of organisms having about 10,000 species include jellyfish, corals and sea anemones. Jellyfish swarms are widespread and frequent in coastal areas worldwide and considered as menace due to their ecological and socio economic consequences (Stabili et al., 2020)

Mcl-1 determines the Bax dependency of Nbk/Bik-induced apoptosis

B cell lymphoma 2 (Bcl-2) homology domain 3 (BH3)–only proteins of the Bcl-2 family are important functional adaptors that link cell death signals to the activation of Bax and/or Bak. The BH3-only protein Nbk/Bik induces cell death via an entirely Bax-dependent/Bak-independent mechanism. In contrast, cell death induced by the short splice variant of Bcl-x depends on Bak but not Bax. This indicates that Bak is functional but fails to become activated by Nbk. Here, we show that binding of myeloid cell leukemia 1 (Mcl-1) to Bak persists after Nbk expression and inhibits Nbk-induced apoptosis in Bax-deficient cells. In contrast, the BH3-only protein Puma disrupts Mcl-1–Bak interaction and triggers cell death via both Bax and Bak. Targeted knockdown of Mcl-1 overcomes inhibition of Bak and allows for Bak activation by Nbk. Thus, Nbk is held in check by Mcl-1 that interferes with activation of Bak. The finding that different BH3-only proteins rely specifically on Bax, Bak, or both has important implications for the design of anticancer drugs targeting Bcl-2

Reproductive dysfunction in the edible oyster, Crassostrea madrasensis due to larval bucephalid infection – a case study

The present case study provides an insight into the tissue level pathological alterations inflicted by Bucephalus sp. infections in the edible oyster, Crassostrea madrasensis. Oysters collected during a routine study (from the oyster beds along the Southeast coast of India during July 2012) was found to harbor larval bucephalid infection. Though the prevalence of infection was low (1.37%), the intensity of infection was high, rated as two on the semi-quantitative scale. Infected oyster did not exhibit any external manifestation, but the developing parasitic stages, after replacing the host gonadal tissues have further spread to the gills and digestive glands. Regions of gonadal tissues were found packed with slender, branching sporocysts containing germ balls and crecariae, destroying the acinar architecture of the gonads. Immune responses like encapsulation against the infective stages were totally absent. The altered acinar architecture and reduced volume of the gonadal acini appeared to be insufficient to support any gametic release, resulting in gonadal dysfunction leading to parasitic castration of the host. An increase in the prevalence of Bucephalus sp. infection in the ecosystem could seriously hamper the reproductive potential of the wild stocks of oysters, thereby affecting the viability of oyster farming in the region

Reproductive dysfunction in the edible oyster, Crassostrea madrasensis due to larval bucephalid infection -a case study Original Article

Abstract The present case study provides an insight into the tissue level pathological alterations inflicted by Bucephalus sp. infections in the edible oyster, Crassostrea madrasensis. Oysters collected during a routine study (from the oyster beds along the Southeast coast of India during July 2012) was found to harbor larval bucephalid infection. Though the prevalence of infection was low (1.37%), the intensity of infection was high, rated as two on the semi-quantitative scale. Infected oyster did not exhibit any external manifestation, but the developing parasitic stages, after replacing the host gonadal tissues have further spread to the gills and digestive glands. Regions of gonadal tissues were found packed with slender, branching sporocysts containing germ balls and crecariae, destroying the acinar architecture of the gonads. Immune responses like encapsulation against the infective stages were totally absent. The altered acinar architecture and reduced volume of the gonadal acini appeared to be insufficient to support any gametic release, resulting in gonadal dysfunction leading to parasitic castration of the host. An increase in the prevalence of Bucephalus sp. infection in the ecosystem could seriously hamper the reproductive potential of the wild stocks of oysters, thereby affecting the viability of oyster farming in the region

Bacterial foraging-optimized PID control of a two-wheeled machine with a two-directional handling mechanism

This paper presents the performance of utilizing a bacterial foraging optimization algorithm on a PID control scheme for controlling a five DOF two-wheeled robotic machine with two-directional handling mechanism. The system under investigation provides solutions for industrial robotic applications that require a limited-space working environment. The system nonlinear mathematical model, derived using Lagrangian modeling approach, is simulated in MATLAB/Simulink(®) environment. Bacterial foraging-optimized PID control with decoupled nature is designed and implemented. Various working scenarios with multiple initial conditions are used to test the robustness and the system performance. Simulation results revealed the effectiveness of the bacterial foraging-optimized PID control method in improving the system performance compared to the PID control scheme

DNA resection in eukaryotes: deciding how to fix the break

DNA double-strand breaks are repaired by different mechanisms, including homologous recombination and nonhomologous end-joining. DNA-end resection, the first step in recombination, is a key step that contributes to the choice of DSB repair. Resection, an evolutionarily conserved process that generates single-stranded DNA, is linked to checkpoint activation and is critical for survival. Failure to regulate and execute this process results in defective recombination and can contribute to human disease. Here, I review recent findings on the mechanisms of resection in eukaryotes, from yeast to vertebrates, provide insights into the regulatory strategies that control it, and highlight the consequences of both its impairment and its deregulation

A System-Wide Investigation of the Dynamics of Wnt Signaling Reveals Novel Phases of Transcriptional Regulation

Aberrant Wnt signaling has been implicated in a wide variety of cancers and many components of the Wnt signaling network have now been identified. Much less is known, however, about how these proteins are coordinately regulated. Here, a broad, quantitative, and dynamic study of Wnt3a-mediated stimulation of HEK 293 cells revealed two phases of transcriptional regulation: an early phase in which signaling antagonists were downregulated, providing positive feedback, and a later phase in which many of these same antagonists were upregulated, attenuating signaling. The dynamic expression profiles of several response genes, including MYC and CTBP1, correlated significantly with proliferation and migration (P<0.05). Additionally, their levels tracked with the tumorigenicity of colon cancer cell lines and they were significantly overexpressed in colorectal adenocarcinomas (P<0.05). Our data highlight CtBP1 as a transcription factor that contributes to positive feedback during the early phases of Wnt signaling and serves as a novel marker for colorectal cancer progression

Return and Volatility Spillovers of Asian Pacific Stock Markets’ Energy Indices

The aim of the study was to investigate the presence of volatility among the Energy Indices of Asia Pacific Stock Markets. To test the volatility among the daily returns of Energy Indices of Asia Pacific Stock Markets, the study selected five sample Asian Pacific stock markets’ Energy Indices on the basis of availability of data. The findings of descriptive statistics and the ADF Test revealed, that the daily returns of the sample energy indices of Asian Pacific stock markets were not normally distributed and achieved stationarity at level difference, over the research period. Hence the data may be used for additional analysis. The data were then analysed, by using the GARCH (1,1) model to assess the considerable volatility of daily returns of sample energy indices and the study, which revealed that during the study period, all of the sample energy indices were volatile

Modulation of enhancer looping and differential gene targeting by Epstein-Barr virus transcription factors directs cellular reprogramming

Epstein-Barr virus (EBV) epigenetically reprogrammes B-lymphocytes to drive immortalization and facilitate viral persistence. Host-cell transcription is perturbed principally through the actions of EBV EBNA 2, 3A, 3B and 3C, with cellular genes deregulated by specific combinations of these EBNAs through unknown mechanisms. Comparing human genome binding by these viral transcription factors, we discovered that 25% of binding sites were shared by EBNA 2 and the EBNA 3s and were located predominantly in enhancers. Moreover, 80% of potential EBNA 3A, 3B or 3C target genes were also targeted by EBNA 2, implicating extensive interplay between EBNA 2 and 3 proteins in cellular reprogramming. Investigating shared enhancer sites neighbouring two new targets (WEE1 and CTBP2) we discovered that EBNA 3 proteins repress transcription by modulating enhancer-promoter loop formation to establish repressive chromatin hubs or prevent assembly of active hubs. Re-ChIP analysis revealed that EBNA 2 and 3 proteins do not bind simultaneously at shared sites but compete for binding thereby modulating enhancer-promoter interactions. At an EBNA 3-only intergenic enhancer site between ADAM28 and ADAMDEC1 EBNA 3C was also able to independently direct epigenetic repression of both genes through enhancer-promoter looping. Significantly, studying shared or unique EBNA 3 binding sites at WEE1, CTBP2, ITGAL (LFA-1 alpha chain), BCL2L11 (Bim) and the ADAMs, we also discovered that different sets of EBNA 3 proteins bind regulatory elements in a gene and cell-type specific manner. Binding profiles correlated with the effects of individual EBNA 3 proteins on the expression of these genes, providing a molecular basis for the targeting of different sets of cellular genes by the EBNA 3s. Our results therefore highlight the influence of the genomic and cellular context in determining the specificity of gene deregulation by EBV and provide a paradigm for host-cell reprogramming through modulation of enhancer-promoter interactions by viral transcription factors