اشترك بالحزمة الذهبية واحصل على وصول غير محدود شمرا أكاديميا
تسجيل مستخدم جديدCorrelated Phenotypic Transitions to Competence in Bacterial Colonies
135
0
0.0
(
0
)
تأليف
Inbal Hecht
اسأل ChatGPT حول البحث
ﻻ يوجد ملخص باللغة العربية
Genetic competence is a phenotypic state of a bacterial cell in which it is capable of importing DNA, presumably to hasten its exploration of alternate genes in its quest for survival under stress. Recently, it was proposed that this transition is uncorrelated among different cells in the colony. Motivated by several discovered signaling mechanisms which create colony-level responses, we present a model for the influence of quorum-sensing signals on a colony of B. Subtilis cells during the transition to genetic competence. Coupling to the external signal creates an effective inhibitory mechanism, which results in anti-correlation between the cycles of adjacent cells. We show that this scenario is consistent with the specific experimental measurement, which fails to detect some underlying collective signaling mechanisms. Rather, we suggest other parameters that should be used to verify the role of a quorum-sensing signal. We also study the conditions under which phenotypic spatial patterns may emerge.
قيم البحث
اقرأ أيضاً
Cell tracking enables data extraction from time-lapse cell movies and promotes modeling biological processes at the single-cell level. We introduce a new fully automated computational strategy to track accurately cells across frames in time-lapse mov
ies. Our method is based on a dynamic neighborhoods formation and matching approach, inspired by motion estimation algorithms for video compression. Moreover, it exploits divide and conquer opportunities to solve effectively the challenging cells tracking problem in overcrowded bacterial colonies. Using cell movies generated by different labs we demonstrate that the accuracy of the proposed method remains very high (exceeds 97%) even when analyzing large overcrowded microbial colonies.
Colonies of bacterial cells endowed with a pili-based self-propulsion machinery represent an ideal model system for studying how active adhesion forces affect structure and dynamics of many-particle systems. As a novel computational tool, we describe
here a highly parallel molecular dynamics simulation package for modeling of textit{Neisseria gonorrhoeae} colonies. Simulations are employed to investigate growth of bacterial colonies and the dependence of the colony structure on cell-cell interactions. In agreement with experimental data, active pilus retraction is found to enhance local ordering. For mixed colonies consisting of different types of cell types, the simulations show a segregation of cell types depending on the pili-mediated interactions, as seen in experiments. Using a simulated experimental setup, we study the power-spectral density of colony-shape fluctuations and the associated fluctuation-response relation. The simulations predict a strong violation of the equilibrium fluctuation-response relation across the measurable frequency range. Lastly, we illustrate the essential role of active force generation for colony dynamics by showing that pilus-mediated activity drives the spreading of colonies on surfaces and the invasion of narrow channels.
System-level properties of metabolic networks may be the direct product of natural selection or arise as a by-product of selection on other properties. Here we study the effect of direct selective pressure for growth or viability in particular enviro
nments on two properties of metabolic networks: latent versatility to function in additional environments and carbon usage efficiency. Using a Markov Chain Monte Carlo (MCMC) sampling based on Flux Balance Analysis (FBA), we sample from a known biochemical universe random viable metabolic networks that differ in the number of directly constrained environments. We find that the latent versatility of sampled metabolic networks increases with the number of directly constrained environments and with the size of the networks. We then show that the average carbon wastage of sampled metabolic networks across the constrained environments decreases with the number of directly constrained environments and with the size of the networks. Our work expands the growing body of evidence about nonadaptive origins of key functional properties of biological networks.
Phenotype transition takes place in many biological processes such as differentiation, and understanding how a cell reprograms its global gene expression profile is a problem of rate theories. A cell phenotype transition accompanies with switching of
expression rates of clusters of genes, analogous to domain flipping in an Ising system. Here through analyzing single cell RNA sequencing data in the framework of transition path theory, we set to study how such a genome-wide expression program switching proceeds in three different cell transition processes. For each process after reconstructing a Markov transition model in the cell state space, we formed an ensemble of shortest paths connecting the initial and final cell states, reconstructed a reaction coordinate describing the transition progression, and inferred the gene regulation network (GRN) along the reaction coordinate. In all three processes we observed common pattern that the frustration of gene regulatory network (GRN), defined as overall confliction between the regulation received by genes and their expression states, first increases then decreases when approaching a new phenotype. The results support a mechanism of concerted silencing of genes that are active in the initial phenotype and activation of genes that are active in the final phenotype.
By challenging E. coli with sublethal norfloxacin for 10 days, Henry Lee and James Collins suggests the bacterial altruism leads to the population-wide resistance. By detailedly analyzing experiment data, we suggest that bacterial cooperation leads t
o population-wide resistance under norfloxacin pressure and simultaneously propose the bacteria shield is the possible feedback mechanism of less resistant bacteria. The bacteria shield is that the less resistant bacteria sacrifice the large number of themselves to consume norfloxacin and then to relieve the norfloxacin burden from highly resistant bacteria. Thus, due to highly resistant bacteria and less resistant bacteria extracted from the same bacteria population, bacterial cooperation leads to heteroresistance.
سجل دخول لتتمكن من نشر تعليقات
التعليقات
جاري جلب التعليقات
سجل دخول لتتمكن من متابعة معايير البحث التي قمت باختيارها
