Opini Komunitas Warga Sekitar Tentang Maraknya Pedagang Kaki Lima (PKL) (Studi Deskriptif Analitis Tentang Opini Komunitas Warga Sekitar Pkl – Tamansari, Kepatihan, dan Dalem Kaum – Kota Bandung)

Penelitian dengan judul “Opini komunitas warga sekitar tentang maraknya Pedagang Kaki Lima (PKL)” ini, dilakukan oleh pengajar/dosen tetap Fakultas Ilmu Komunikasi (FIK). Permasalahan penelitian adalah tentang bagaimana opini komunitas warga sekitar PKL mengenai keamanan, ketertiban, ketenangan, Kenyamanan, keindahan, kebersihan, dan keramah-tamahan (7“K”) akibat maraknya PKL. Sasaran strategis dalam penelitian ini adalah komunitas warga di sekitar lingkungan PKL Jalan Kepatihan, Dalem Kaum, dan Tamansari.Tujuan penelitian adalah untuk mengetahui, mengkaji, dan menganalisis faktor 7“K” yang dirasakan komunitas warga sekitar, akibat maraknya PKL, sehingga tanggapan yang diekspresikan mereka dapat menjadi masukan bagi Humas Pemerintah Kota Bandung dalam upaya mensosialisasikan kebijakan pemerintah tentang PKL khususnya dalam merumuskan konsep community relations berkaitan dengan 7 “K” yang dirasakan oleh komunitas warga sekitar terhadap maraknya PKL tersebut. Kesimpulan hasil penelitian ini adalah: pada umumnya opini komunitas warga sekitar terhadap maraknya PKL, dilihat dari faktor 7“K” sangatlah bervariasi di antara opini positif dan negatif, Dalam arti, untuk responden tertentu penilaiannya sangat relatif tergantung dari persepsi masing-masing dan atas dasar pengalaman masing-masing dengan para PKL tersebut. Dengan demikian tidak sepenuhnya berada pada kecenderungan tertentu yang bersifat negatif atau positif. Oleh karena itu dari opini tersebut selanjutnya dapat berkembang untuk diyakini tentang adanya kemungkinan di antara kedua belah pihak saling membina hubungan, dan pemerintah memfasilitasi hubungan tersebut dalam kebijakan-kebijakannya

Коло Марусі Чурай

In this article Marusya Churay*s (a character famous in story and song) life history is researched. On the basis of real events and historical facts the author tells about people who were related to the life of this personality

RodZ modulates geometric localization of the bacterial actin MreB to regulate cell shape

Membrane protein RodZ interacts with the actin-like protein MreB, which coordinates cell-wall insertion to maintain the typical rod-like shape of E. coli cells. Here, the authors provide evidence that RodZ modulates the biophysical properties of MreB and alters the spatial organization of cell-wall growth

Coupling between Protein Stability and Catalytic Activity Determines Pathogenicity of G6PD Variants

G6PD deficiency, an enzymopathy affecting 7% of the world population, is caused by over 160 identified amino acid variants in glucose-6-phosphate dehydrogenase (G6PD). The clinical presentation of G6PD deficiency is diverse, likely due to the broad distribution of variants across the protein and the potential for multidimensional biochemical effects. In this study, we use bioinformatic and biochemical analyses to interpret the relationship between G6PD variants and their clinical phenotype. Using structural information and statistical analyses of known G6PD variants, we predict the molecular phenotype of five uncharacterized variants from a reference population database. Through multidimensional analysis of biochemical data, we demonstrate that the clinical phenotypes of G6PD variants are largely determined by a trade-off between protein stability and catalytic activity. This work expands the current understanding of the biochemical underpinnings of G6PD variant pathogenicity and suggests a promising avenue for correcting G6PD deficiency by targeting essential structural features of G6PD

Conservation of conformational dynamics across prokaryotic actins.

The actin family of cytoskeletal proteins is essential to the physiology of virtually all archaea, bacteria, and eukaryotes. While X-ray crystallography and electron microscopy have revealed structural homologies among actin-family proteins, these techniques cannot probe molecular-scale conformational dynamics. Here, we use all-atom molecular dynamic simulations to reveal conserved dynamical behaviors in four prokaryotic actin homologs: MreB, FtsA, ParM, and crenactin. We demonstrate that the majority of the conformational dynamics of prokaryotic actins can be explained by treating the four subdomains as rigid bodies. MreB, ParM, and FtsA monomers exhibited nucleotide-dependent dihedral and opening angles, while crenactin monomer dynamics were nucleotide-independent. We further show that the opening angle of ParM is sensitive to a specific interaction between subdomains. Steered molecular dynamics simulations of MreB, FtsA, and crenactin dimers revealed that changes in subunit dihedral angle lead to intersubunit bending or twist, suggesting a conserved mechanism for regulating filament structure. Taken together, our results provide molecular-scale insights into the nucleotide and polymerization dependencies of the structure of prokaryotic actins, suggesting mechanisms for how these structural features are linked to their diverse functions

Extracting phylogenetic dimensions of coevolution reveals hidden functional signals

International audienceDespite the structural and functional information contained in the statistical coupling between pairs of residues in a protein, coevolution associated with function is often obscured by artifactual signals such as genetic drift, which shapes a protein’s phylogenetic history and gives rise to concurrent variation between protein sequences that is not driven by selection for function. Here, we introduce a background model for phylogenetic contributions of statistical coupling that separates the coevolution signal due to inter-clade and intra-clade sequence comparisons and demonstrate that coevolution can be measured on multiple phylogenetic timescales within a single protein. Our method, nested coevolution (NC), can be applied as an extension to any coevolution metric. We use NC to demonstrate that poorly conserved residues can nonetheless have important roles in protein function. Moreover, NC improved the structural-contact predictions of several coevolution-based methods, particularly in subsampled alignments with fewer sequences. NC also lowered the noise in detecting functional sectors of collectively coevolving residues. Sectors of coevolving residues identified after application of NC were more spatially compact and phylogenetically distinct from the rest of the protein, and strongly enriched for mutations that disrupt protein activity. Thus, our conceptualization of the phylogenetic separation of coevolution provides the potential to further elucidate relationships among protein evolution, function, and genetic diseases

Systematic Perturbation of Cytoskeletal Function Reveals a Linear Scaling Relationship between Cell Geometry and Fitness

Diversification of cell size is hypothesized to have occurred through a process of evolutionary optimization, but direct demonstrations of causal relationships between cell geometry and fitness are lacking. Here, we identify a mutation from a laboratory-evolved bacterium that dramatically increases cell size through cytoskeletal perturbation and confers a large fitness advantage. We engineer a library of cytoskeletal mutants of different sizes and show that fitness scales linearly with respect to cell size over a wide physiological range. Quantification of the growth rates of single cells during the exit from stationary phase reveals that transitions between “feast-or-famine” growth regimes are a key determinant of cell-size-dependent fitness effects. We also uncover environments that suppress the fitness advantage of larger cells, indicating that cell-size-dependent fitness effects are subject to both biophysical and metabolic constraints. Together, our results highlight laboratory-based evolution as a powerful framework for studying the quantitative relationships between morphology and fitness

Additional file 4: Figure S4. of Rapid, precise quantification of bacterial cellular dimensions across a genomic-scale knockout library

Morphological analysis of the Keio collection reveals correlations between cell width and intracellular width variability. Contours from cells from each Keio deletion strain were extracted from images acquired from the NBRP repository and used to compute the mean width and width profile across each cell. For each cell, we then computed the standard deviation of the width profile divided by the mean width to obtain the intracellular width variability. White circles and error bars were obtained by binning strains by mean width; blue lines are the fit to binned averages. R is Pearson’s correlation coefficient; p-value was computed with Student’s t-test. (PDF 111 kb

Additional file 6: Table S1. of Rapid, precise quantification of bacterial cellular dimensions across a genomic-scale knockout library

Conditions in chemical genomics screen from [29] that exhibit negative correlation between mean cell width and S-score with p-value less than 0.000154 (Bonferroni multiple-hypothesis correction to p < 0.05 across 324 conditions; see Methods). Table S2. Conditions in chemical genomics screen from [29] that exhibit positive correlation between mean cell width and S-score with p-value less than 0.000154 (Bonferroni multiple-hypothesis correction to p < 0.05 across 324 conditions; see Methods). Table S3. Pairs of COGs and conditions in chemical genomics screen from [29] that exhibit correlations between mean cell width and S-scores with p-value less than 0.000154 (Bonferroni multiple-hypothesis correction to p < 0.05 across 324 conditions; see Methods). *: description from [29] and generously provided by Athanasios Typas. Table S4. Pairs of COGs and conditions in chemical genomics screen from [29] that exhibit correlations between mean cell length and S-scores with p-value less than 0.000154 (Bonferroni multiple-hypothesis correction to p < 0.05 across 324 conditions; see Methods). *: description from [29] and generously provided by Athanasios Typas. (DOCX 101 kb

Systematically testing human HMBS missense variants to reveal mechanism and pathogenic variation

Defects in hydroxymethylbilane synthase (HMBS) can cause Acute Intermittent Porphyria (AIP), an acute neurological disease. Although sequencing-based diagnosis can be definitive, ~⅓ of clinical HMBS variants are missense variants, and most clinically-reported HMBS missense variants are designated as "variants of uncertain significance" (VUS). Using saturation mutagenesis, en masse selection, and sequencing, we applied a multiplexed validated assay to both the erythroid-specific and ubiquitous isoforms of HMBS, obtaining confident functional impact scores for >84% of all possible amino-acid substitutions. The resulting variant effect maps generally agreed with biochemical expectation. However, the maps showed variants at the dimerization interface to be unexpectedly well tolerated, and suggested residue roles in active site dynamics that were supported by molecular dynamics simulations. Most importantly, these HMBS variant effect maps can help discriminate pathogenic from benign variants, proactively providing evidence even for yet-to-be-observed clinical missense variants