Mangrove root: adaptations and ecological importance

Key message

This review gives a comprehensive overview of adaptations of mangrove root system to the adverse environmental conditions and summarizes the ecological importance of mangrove root to the ecosystem.

Abstract

In plants, the first line of defense against abiotic stress is in their roots. If the soil surrounding the plant root is healthy and biologically diverse, the plant will have a higher chance to survive in stressful conditions. Different plant species have unique adaptations when exposed to a variety of abiotic stress conditions. None of the responses are identical, even though plants have become adapted to the exact same environment. Mangrove plants have developed complex morphological, anatomical, physiological, and molecular adaptations allowing survival and success in their high-stress habitat. This review briefly depicts adaptive strategies of mangrove roots with respect to anatomy, physiology, biochemistry and also the major advances recently made at the genetic and genomic levels. Results drawn from the different studies on mangrove roots have further indicated that specific patterns of gene expression might contribute to adaptive evolution of mangroves under high salinity. We also review crucial ecological contributions provided by mangrove root communities to the ecosystem including marine fauna.

     

Induction of sex reversal in Oreochromis mossambicus by diethylstilbestrol

The efficacy of the synthetic estrogen, diethylstilbestrol (DES), for sex-reversal in the Java tilapia, Oreochromis mossambicus was investigated. Fry of 8–10 mm total length were fed diets containing 25, 50 and 100 ppm of DES for 30 days in plastic pools; this was followed by 45–65 days rearing in fertilized cement cisterns where hormone-free diet was given. DES at 50 and 100 ppm induced 100% sex-reversal; DES at 25 ppm resulted in only a slightly larger proportion of females to males. The untreated control group had a higher proportion of males than females. No intersex or sterile individuals were observed among the steroid-treated fish. The present investigation demonstrates that 50 ppm DES administered for 30 days is sufficient to induce a 100% sex-reversal in O. mossambicus.     

Development of a new bioprocess scheme using frozen seed train intermediates to initiate CHO cell culture manufacturing campaigns

Agility to schedule and execute cell culture manufacturing campaigns quickly in a multi‐product facility will play a key role in meeting the growing demand for therapeutic proteins. In an effort to shorten campaign timelines, maximize plant flexibility and resource utilization, we investigated the initiation of cell culture manufacturing campaigns using CHO cells cryopreserved in large volume bags in place of the seed train process flows that are conventionally used in cell culture manufacturing. This approach, termed FASTEC (Frozen Accelerated Seed Train for Execution of a Campaign), involves cultivating cells to high density in a perfusion bioreactor, and cryopreserving cells in multiple disposable bags. Each run for a manufacturing campaign would then come from a thaw of one or more of these cryopreserved bags. This article reviews the development and optimization of individual steps of the FASTEC bioprocess scheme: scaling up cells to greater than 70 × 10⁶ cells/mL and freezing in bags with an optimized controlled rate freezing protocol and using a customized rack configuration. Flow cytometry analysis was also employed to understand the recovery of CHO cells following cryopreservation. Extensive development data were gathered to ensure that the quantity and quality of the drug manufactured using the FASTEC bioprocess scheme was acceptable compared to the conventional seed train process flow. The result of offering comparable manufacturing options offers flexibility to the cell culture manufacturing network. Biotechnol. Bioeng. 2013; 110: 1376–1385. © 2012 Wiley Periodicals, Inc.     

Mutation of the LXCXE Binding Cleft of pRb Facilitates Transformation by ras In Vitro but Does Not Promote Tumorigenesis In Vivo

Background

The Retinoblastoma protein (pRB) is a key tumor suppressor that is functionally inactivated in most cancers. pRB regulates the cell division cycle and cell cycle exit through protein–protein interactions mediated by its multiple binding interfaces. The LXCXE binding cleft region of pRB mediates interactions with cellular proteins that have chromatin regulatory functions. Chromatin regulation mediated by pRB is required for a stress responsive cell cycle arrest, including oncogene induced senescence. The in vivo role of chromatin regulation by pRB during senescence, and its relevance to cancer is not clear.

Methodology/Principal Findings

Using gene-targeted mice, uniquely defective for pRB mediated chromatin regulation, we investigated its role during transformation and tumor progression in response to activation of oncogenic ras. We report that the pRB^∆L mutation confers susceptibility to escape from HrasV12 induced senescence and allows transformation in vitro, although these cells possess high levels of DNA damage. Intriguingly, LSL-Kras, Rb1 ^∆L/∆L mice show delayed lung tumor formation compared to controls. This is likely due to the increased apoptosis seen in the early hyperplastic lesions shortly following ras activation that inhibits tumor progression. Furthermore, DMBA treatment to induce sporadic ras mutations in other tissues also failed to reveal greater susceptibility to cancer in Rb1 ^∆L/∆L mice.

Conclusions/Significance

Our data suggests that chromatin regulation by pRB can function to limit proliferation, but its loss fails to contribute to cancer susceptibility in ras driven tumor models because of elevated levels of DNA damage and apoptosis.     

Identification of GR and TrxR systems in Setaria cervi: Purification and characterization of glutathione reductase

The glutathione reductase (GR) and thioredoxin reductase (TrxR) are important enzymes of the redox system that aid parasites to maintain an adequate intracellular redox environment. In the present study, the enzyme activity of GR and TrxR was investigated in Setaria cervi (S. cervi). Significant activity of both enzymes was detected in the somatic extract of adult and microfilariae stages of S. cervi. Both GR and TrxR were separated by partial purification using ammonium sulfate fractionation and DEAE ion exchange chromatography suggesting the presence of both glutathione and thioredoxin systems in S. cervi. The enzyme glutathione reductase (ScGR) was purified to homogeneity using affinity and ion exchange chromatography that resulted in 90 fold purification with a yield of 11.54%. The specific activity of the ScGR was 643 U/mg that migrated as a single band on SDS-PAGE. The subunit molecular mass was determined to be ~ 50 kDa while the optimum pH and temperature were found to be 7.0 and 35 °C respectively. The activation energy (Ea) was calculated from the slope of Arrhenius plot as 16.29 ± 1.40 kcal/mol. The Km and Vmax were determined to be 0.27 ± 0.045 mM; 30.30 ± 1.30 U/ml with NADPH and 0.59 ± 0.060 mM; 4.16 ± 0.095 U/ml with GSSG respectively. DHBA, a specific inhibitor for GR has completely inhibited the enzyme activity at 1 μM concentration. The inhibition of ScGR activity with NAI (IC₅₀ 0.71 mM), NEM (IC₅₀ 0.50 mM) and DEPC (IC₅₀ 0.27 mM) suggested the presence of tyrosine, cysteine and histidine residues at its active site. Further studies on characterization and understanding of these antioxidant enzymes may lead to designing of an effective drug against lymphatic filariasis.     

Ectopic expression of a Drosophila InsP(3)R channel mutant has dominant-negative effects in vivo.

The inositol 1,4,5-trisphosphate (InsP(3)) receptor is a tetrameric intracellular calcium channel. It is an integral component of the InsP(3) signaling pathway in multicellular organisms, where it regulates cellular calcium dynamics in many different contexts. In order to understand how the primary structure of the InsP(3)R affects its functional properties, the kinetics of Ca(2+)-release in vitro from single point mutants of the Drosophila InsP(3)R have been determined earlier. Among these, the Ka901 mutant in the putative selectivity-filter of the pore is of particular interest. It is non-functional in the homomeric form whereas it forms functional channels (with altered channel properties) when co-expressed with wild-type channels. Here we show that due to its changed functional properties the Ka901 mutant protein has dominant-negative effects in vivo. Cells expressing Ka901:WT channels exhibit much higher levels of cytosolic Ca(2+) upon stimulation as compared with cells over-expressing just the wild-type DmInsP(3)R, thus supporting our in vitro observations that increased Ca(2+) release is a property of heteromeric Ka901:WT channels. Furthermore, ectopic expression of the Ka901 mutant channel in aminergic cells of Drosophila alters electrophysiological properties of a flight circuit and results in defective flight behavior.     

Coronin 1B supports RhoA signaling at cell-cell junctions through Myosin II

Non-muscle myosin II (NMII) motor proteins are responsible for generating contractile forces inside eukaryotic cells. There is also a growing interest in the capacity for these motor proteins to influence cell signaling through scaffolding, especially in the context of RhoA GTPase signaling. We previously showed that NMIIA accumulation and stability within specific regions of the cell cortex, such as the zonula adherens (ZA), allows the formation of a stable RhoA signaling zone. Now we demonstrate a key role for Coronin 1B in maintaining this junctional pool of NMIIA, as depletion of Coronin 1B significantly compromised myosin accumulation and stability at junctions. The loss of junctional NMIIA, upon Coronin 1B knockdown, perturbed RhoA signaling due to enhanced junctional recruitment of the RhoA antagonist, p190B Rho GAP. This effect was blocked by the expression of phosphomimetic MRLC-DD, thus reinforcing the central role of NMII in regulating RhoA signaling.     

Short- and long-term outcomes in infective endocarditis patients: a systematic review and meta-analysis

Background

Despite advances in medical knowledge, technology and antimicrobial therapy, infective endocarditis (IE) is still associated with devastating outcomes. No reviews have yet assessed the outcomes of IE patients undergoing short- and long-term outcome evaluation, such as all-cause mortality and IE-related complications. We conducted a systematic review and meta-analysis to examine the short- and long-term mortality, as well as IE-related complications in patients with definite IE.

Methods

A computerized systematic literature search was carried out in PubMed, Scopus and Google Scholar from 2000 to August, 2016. Included studies were published studies in English that assessed short-and long-term mortality for adult IE patients. Pooled estimations with 95% confidence interval (CI) were calculated with DerSimonian-Laird (DL) random-effects model. Sensitivity and subgroup analyses were also performed. Publication bias was evaluated using inspection of funnel plots and statistical tests.

Results

Twenty five observational studies (retrospective, 14; prospective, 11) including 22,382 patients were identified. The overall pooled mortality estimates for IE patients who underwent short- and long-term follow-up were 20% (95% CI: 18.0–23.0, P?<?0.01) and 37% (95% CI: 27.0–48.0, P?<?0.01), respectively. The pooled prevalence of cardiac complications in patients with IE was found to be 39% (95%CI: 32.0–46.0) while septic embolism and renal complications accounted for 25% (95% CI: 20.0–31) and 19% (95% CI: 14.0–25.0) (all P?<?0.01), respectively.

Conclusion

Irrespective of the follow-up period, a significantly higher mortality rate was reported in IE patients, and the burden of IE-related complications were immense. Further research is needed to assess the determinants of overall mortality in IE patients, as well as well-designed observational studies to conform our results.

     

Synthesis and biological evaluation of estradiol linked pyrrolo[2,1-c][1,4]benzodiazepine (PBD) conjugates as potential anticancer agents

A series of new estradiol linked pyrrolo[2,1-c][1,4]benzodiazepine (E(2)-PBD) conjugates (3a-f, 4a-f and 5a-f) with different linker architectures including a triazole moiety have been designed and synthesized. All the 18 compounds have been evaluated for their anticancer activity and it is observed that some of the compounds particularly 4c-e and 5c,d exhibited significant anticancer activity. The detailed biological aspects relating to the cell cycle effects and tubulin depolymerization activity have been examined with a view to understand the mechanism of action of these conjugates. Among all these conjugates, one of the compound 5c could be considered as the most effective compound particularly against MCF-7 breast cancer cell line.