A new role for PGRP-S (Tag7) in immune defense: lymphocyte migration is induced by a chemoattractant complex of Tag7 with Mts1

PGRP-S (Tag7) is an innate immunity protein involved in the antimicrobial defense systems, both in insects and in mammals. We have previously shown that Tag7 specifically interacts with several proteins, including Hsp70 and the calcium binding protein S100A4 (Mts1), providing a number of novel cellular functions. Here we show that Tag7–Mts1 complex causes chemotactic migration of lymphocytes, with NK cells being a preferred target. Cells of either innate immunity (neutrophils and monocytes) or acquired immunity (CD4⁺ and CD8⁺ lymphocytes) can produce this complex, which confirms the close connection between components of the 2 branches of immune response.     

Mitochondria-targeted plastoquinone derivative SkQ1 increases early reproduction of <Emphasis Type="Italic">Drosophila melanogaster</Emphasis> at the cost of early survival

It was previously found that 20 pM SkQ1 (10-(6′-plastoquinonyl) decyltriphenylphosphonium) solution increased lifespan of virgin females and males of the fruit fly Drosophila melanogaster with maximal and highly reproducible effect on early survival of females. In this paper we demonstrate that SkQ1 solution of the same concentration does not increase lifespan of mated females and males, early effect on female survival being absent, whereas early fertility and the total number of progeny are elevated in treated flies. Increase in fertility observed in young mated females instead of increase of survival typical for young virgin females might illustrate the trade-off between the fly’s lifespan and reproduction.     

Heterochromatic DNA repeats in <Emphasis Type="Italic">Drosophila</Emphasis> and unusual gene silencing in yeast cells

The 1.25-kb heterochromatic Stellate repeats of Drosophila melanogaster are capable of stably persisting in transgenic constructs and silencing the white reporter gene (mosaic position effect variegation). This system reveals an unusual form of silencing, which is insensitive to known modifiers of position effect variegation. The unusual form of silencing was studied with yeast Saccharomyces cerevisiae, a simple eukaryotic model. To be transferred into yeast cells, the D. melanogaster Stellate repeats were cloned in the pYAC4 centromeric vector (CEN4, URA3, TRP1, HIS3). The HIS3 and/or URA3 genes could be inactive in plasmids consisting of pYAC4 and the Stellate insert in yeast cells. Deletion of D. melanogaster DNA from the plasmid was found to activate the URA3 and HIS3 genes. It was assumed that the genes were repressed rather than damaged in the presence of the Stellate repeats and that a new form of gene silencing was revealed in.     

AmylPepPred: Amyloidogenic Peptide Prediction tool

We present an efficient computational architecture designed using supervised machine learning model to predict amyloid fibril forming protein segments, named AmylPepPred. The proposed prediction model is based on bio-physio-chemical properties of primary sequences and auto-correlation function of their amino acid indices. AmylPepPred provides a user friendly web interface for the researchers to easily observe the fibril forming and non-fibril forming hexmers in a given protein sequence. We expect that this stratagem will be highly encouraging in discovering fibril forming regions in proteins thereby benefit in finding therapeutic agents that specifically aim these sequences for the inhibition and cure of amyloid illnesses.

Availability

AmylPepPred is available freely for academic use at www.zoommicro.in/amylpeppred     

Interaction between checkpoint genes RAD9, RAD17, RAD24, RAD53, and genes SRM5/CDC28, SRM8/NET1, and SRM12/HFI1 involved in the determination of yeast Saccharomyces cerevisiae sensitivity to ionizing radiation

Analysis of radiosensitivity of double mutants in the yeast Saccharomyces cerevisiae revealed that checkpoint genes RAD9, RAD17, RAD24, and RAD53 along with genes CDC28 and NET1 belong to one epistasis group designated the RAD9 group. The use of srm mutations allowed the demonstration of a branched RAD9-dependent pathway of cell radioresistance. Mutation cdc28-srm is hypostatic to rad9Δ, rad17Δ, and rad24Δ being additive with rad53. Mutation net1-srm is hypostatic to rad9Δ and rad53 but additively enhance the effects of mutations rad17Δ and rad24Δ. Gene SRM12/HFI1 is not a member of the RAD9 group. Mutation in gene hfi1-srm manifests the additive effect on mutations rad24Δ and rad9Δ. The analyzed genes can also participate in minor mechanisms of radioresistance that are relatively independent of the above RAD9-dependent mechanism.