Bioinformatics Analysis of Upstream Region and Protein Structure of Fungal Phytase Gene

Phytase increases the bioavailability of phytate phosphorus in seed-based animal feeds and reduces the phosphorus pollution of animal waste. Since most animal feeds for pellets are heated up to 65-80 °C, the production of a thermostable structure for phytase can be useful. In this study, we sought to perform bioinformatics analysis of the upstream region and protein structure of fungal phytase to improve its expression and thermostability properties. We used bioinformatics methods such as similarity search, multiple alignment, statistical analysis of physicochemical properties of amino acids, pattern recognition, and protein modeling to find out the effective factors in heat resistance of phytase. Change in Gibbs free energy (ΔG) of the best pattern promoter resulting from the interaction between RNA polymerase and the promoter sequences of modified genes of phytase was equal to -9 kcalmol-1, which is lower compared to other interactions. The evaluation of the three-dimensional structure of new phytases showed that amino acid substitutions aimed at improving thermostability did not change the form and structure of the protein. The results of Prochek, Whatcheck, and ERRAT for structural analysis and verification were 84, 72, and 70, respectively, that were satisfactory

ECEL1 novel mutation in arthrogryposis type 5D: A molecular dynamic simulation study.

BACKGROUND: ECEL1 has been presented as a causal gene of an autosomal recessive form distal arthrogryposis (DA) which affects the distal joints. The present study focused on bioinformatic analysis of a novel mutation in ECEL1, c.535A>G (p. Lys179Glu), which was reported in a family with 2 affected boys and fetus through prenatal diagnosis. METHODS: Whole-exome sequencing data analyzed followed by molecular dynamic (MD) simulation of native ECEL1 protein and mutant structures using GROMACS software. One variant c.535A>G, p. Lys179Glu (homozygous) on gene ECEL1 has been detected in proband which was validated in all family members through Sanger sequencing. RESULTS: We demonstrated remarkable constructional differences by MD simulation between wild-type and novel mutant of ECEL1 gene. The reason for the lack of the Zn ion binding in mutation in the ECEL1 protein has been identified by average atomic distance and SMD analysis among the wild-type and mutant. CONCLUSION: Overall, in this study, we present knowledge of the effect of the studied variant on the ECEL1 protein leading to neurodegenerative disorder in humans. This work may hopefully be supplementary to classical molecular dynamics to dissolve the mutational effects of cofactor-dependent protein

Stem cell treatment of degenerative eye disease

Stem cell therapies are being explored extensively as treatments for degenerative eye disease, either for replacing lost neurons, restoring neural circuits or, based on more recent evidence, as paracrine-mediated therapies in which stem cell-derived trophic factors protect compromised endogenous retinal neurons from death and induce the growth of new connections. Retinal progenitor phenotypes induced from embryonic stem cells/induced pluripotent stem cells (ESCs/iPSCs) and endogenous retinal stem cells may replace lost photoreceptors and retinal pigment epithelial (RPE) cells and restore vision in the diseased eye, whereas treatment of injured retinal ganglion cells (RGCs) has so far been reliant on mesenchymal stem cells (MSC). Here, we review the properties of non-retinal-derived adult stem cells, in particular neural stem cells (NSCs), MSC derived from bone marrow (BMSC), adipose tissues (ADSC) and dental pulp (DPSC), together with ESC/iPSC and discuss and compare their potential advantages as therapies designed to provide trophic support, repair and replacement of retinal neurons, RPE and glia in degenerative retinal diseases. We conclude that ESCs/iPSCs have the potential to replace lost retinal cells, whereas MSC may be a useful source of paracrine factors that protect RGC and stimulate regeneration of their axons in the optic nerve in degenerate eye disease. NSC may have potential as both a source of replacement cells and also as mediators of paracrine treatment