Meiotic recombination in Drosophila females depends on chromosome continuity between genetically defined boundaries

In the pairing-site model, specialized regions on each chromosome function to establish meiotic homolog pairing. Analysis of these sites could provide insights into the mechanism used by Drosophila females to form a synaptonemal complex (SC) in the absence of meiotic recombination. These specialized sites were first established on the X chromosome by noting that there were barriers to crossover suppression caused by translocation heterozygotes. These sites were genetically mapped and proposed to be pairing sites. By comparing the cytological breakpoints of third chromosome translocations to their patterns of crossover suppression, we have mapped two sites on chromosome 3R. We have performed experiments to determine if these sites have a role in meiotic homolog pairing and the initiation of recombination. Translocation heterozygotes exhibit reduced gene conversion within the crossover-suppressed region, consistent with an effect on the initiation of meiotic recombination. To determine if homolog pairing is disrupted in translocation heterozygotes, we used fluorescent in situ hybridization to measure the extent of homolog pairing. In wild-type oocytes, homologs are paired along their entire lengths prior to accumulation of the SC protein C(3)G. Surprisingly, translocation heterozygotes exhibited homolog pairing similar to wild type within the crossover-suppressed regions. This result contrasted with our observations of c(3)G mutant females, which were found to be defective in pairing. We propose that each Drosophila chromosome is divided into several domains by specialized sites. These sites are not required for homolog pairing. Instead, the initiation of meiotic recombination requires continuity of the meiotic chromosome structure within each of these domains.     

Trends,application and future prospectives of microbial carbonic anhydrase mediated carbonation process for CCUS

Summary

Growing industrialization and the desire for a better economy in countries has accelerated the emission of greenhouse gases (GHGs), by more than the buffering capacity of the earth's atmosphere. Among the various GHGs, carbon dioxide occupies the first position in the anthroposphere and has detrimental effects on the ecosystem. For decarbonization, several non‐biological methods of carbon capture, utilization and storage (CCUS) have been in use for the past few decades, but they are suffering from narrow applicability. Recently, CO₂ emission and its disposal related problems have encouraged the implementation of bioprocessing to achieve a zero waste economy for a sustainable environment. Microbial carbonic anhydrase (CA) catalyses reversible CO₂ hydration and forms metal carbonates that mimic the natural phenomenon of weathering/carbonation and is gaining merit for CCUS. Thus, the diversity and specificity of CAs from different micro‐organisms could be explored for CCUS. In the literature, more than 50 different microbial CAs have been explored for mineral carbonation. Further, microbial CAs can be engineered for the mineral carbonation process to develop new technology. CA driven carbonation is encouraging due to its large storage capacity and favourable chemistry, allowing site‐specific sequestration and reusable product formation for other industries. Moreover, carbonation based CCUS holds five‐fold more sequestration capacity over the next 100 years. Thus, it is an eco‐friendly, feasible, viable option and believed to be the impending technology for CCUS. Here, we attempt to examine the distribution of various types of microbial CAs with their potential applications and future direction for carbon capture. Although there are few key challenges in bio‐based technology, they need to be addressed in order to commercialize the technology.     

Changes in body fluid compartments on re-induction to high altitude and effect of diuretics

Studies were carried out in 29 healthy young adults in the Indian Army stationed in the plains and posted at an elevation of 3500 m for more than 6 months. After exposure to a low elevation in Delhi (260 m) for 3 weeks they were reinduced to a height of 3500 m. The subjects were divided into three groups, each of which was treated with either placebo or acetazolamide or spironolactone. The drug treatment was started immediately after their landing at high altitude and continued for 2 days only. Total body water, extracellular fluid, intracellular fluid, plasma volume, blood pH, PaO₂, PaCO₂ and blood viscosity were determined on exposure at Delhi and on re-induction to high altitude. Plasma volume was increased after the descent from high altitude and remained high for up to 21 day's study. This increased plasma volume may have some significance in the pathogenesis of pulmonary oedema. Total body water and intracellular fluid content were increased at 260 m elevation, while extracellular fluid decreased. On re-induction there was a decrease in total body water with no change in the extracellular fluid content.This paper was presented in part at the 17th annual conference of the Society of Nuclear Medicine, India held at Bangalore, January 2–4, 1986     

MKK3-MPK6-MYC2 module positively regulates ABA biosynthesis and signalling in Arabidopsis

Journal of Plant Biochemistry and Biotechnology - Involvement of MAPK cascades is well studied in the regulation of ABA mediated responses such as stomatal opening, seed germination and stress...     

Classification of videocapsule endoscopy image patterns: comparative analysis between patients with celiac disease and normal individuals

Background  

Quantitative disease markers were developed to assess videocapsule images acquired from celiac disease patients with villous atrophy, and from control patients.     

Synthesis and characterization of pure and Li+ activated Alq3 complexes for green and blue organic light emitting diodes and display devices

Pure and Li⁺‐doped Alq₃ complexes were synthesized by simple precipitation method at room temperature, maintaining the stoichiometric ratio. These complexes were characterized by X‐ray diffraction, ultraviolet‐visible absorption and Fourier transform infrared and photoluminescence (PL) spectra. X‐ray diffraction analysis reveals the crystalline nature of the synthesized complexes, while Fourier transform infrared spectroscopy confirm the molecular structure, the completion of quinoline ring formation and presence of quinoline structure in the metal complex. Ultraviolet‐visible and PL spectra revealed that Li⁺ activated Alq₃ complexes exhibit the highest intensity in comparison to pure Alq₃ phosphor. Thus, Li⁺ enhances PL emission intensity when doped into Alq₃ phosphor. The excitation spectra lie in the range of 383–456 nm. All the synthesized complexes other than Liq give green emission, while Liq gives blue emission with enhanced intensity. Thus, he synthesized phosphors are the best suitable candidates for green‐ and blue‐emitting organic light emitting diode, PL liquid‐crystal display and solid‐state lighting applications. Copyright © 2013 John Wiley & Sons, Ltd.     

Aberrant ROCK activation promotes the development of type I diabetes in NOD mice

Aberrant production of IL-21 by T cells is critical for the development of type 1 diabetes (T1D) in NOD mice. The pathogenic effects of IL-21 are partly due to its ability to promote the generation of T(H)-17 cells. Interferon Regulatory Factor (IRF4) is a crucial regulator of IL-17 and IL-21 production. We recently found that the serine-threonine kinase ROCK2 phosphorylates IRF4 and regulates its ability to control IL-17 and IL-21 production. Here we show that NOD T cells aberrantly activate ROCK2. We furthermore demonstrate that ROCK inhibition corrects the abnormal IRF4 function in NOD T cells and diminishes their production of IL-17 and IL-21. Importantly, administration of a ROCK inhibitor to NOD mice protects against diabetes development. These studies thus support the idea that ROCK2 is inappropriately activated in NOD T cells and that ROCK kinases could represent important therapeutic targets for the treatment of T1D.