Pub Date : 2018-01-01Epub Date: 2017-12-06DOI: 10.18547/gcb.2018.vol4.iss1.e100050
Vidisha Singh, Marek Ostaszewski, George D Kalliolias, Gilles Chiocchia, Robert Olaso, Elisabeth Petit-Teixeira, Tomáš Helikar, Anna Niarakis
In this work we present a systematic effort to summarize current biological pathway knowledge concerning Rheumatoid Arthritis (RA). We are constructing a detailed molecular map based on exhaustive literature scanning, strict curation criteria, re-evaluation of previously published attempts and most importantly experts' advice. The RA map will be web-published in the coming months in the form of an interactive map, using the MINERVA platform, allowing for easy access, navigation and search of all molecular pathways implicated in RA, serving thus, as an on line knowledgebase for the disease. Moreover the map could be used as a template for Omics data visualization offering a first insight about the pathways affected in different experimental datasets. The second goal of the project is a dynamical study focused on synovial fibroblasts' behavior under different initial conditions specific to RA, as recent studies have shown that synovial fibroblasts play a crucial role in driving the persistent, destructive characteristics of the disease. Leaning on the RA knowledgebase and using the web platform Cell Collective, we are currently building a Boolean large scale dynamical model for the study of RA fibroblasts' activation.
在这项工作中，我们系统地总结了当前有关类风湿关节炎（RA）的生物通路知识。我们正在构建一个详细的分子图谱，该图谱基于详尽的文献扫描、严格的编辑标准、对以前发表的尝试的重新评估，以及最重要的专家建议。未来几个月，我们将利用 MINERVA 平台，以交互式地图的形式在网上发布 RA 地图，以便于访问、导航和搜索与 RA 有关的所有分子通路，从而成为该疾病的在线知识库。此外，该地图还可作为 Omics 数据可视化的模板，让人们初步了解不同实验数据集中受影响的通路。该项目的第二个目标是对滑膜成纤维细胞在RA特有的不同初始条件下的行为进行动态研究，因为最近的研究表明，滑膜成纤维细胞在驱动该疾病的持久性和破坏性特征方面发挥着至关重要的作用。借助 RA 知识库和网络平台 Cell Collective，我们目前正在建立一个布尔大规模动力学模型，用于研究 RA 成纤维细胞的活化。
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Pub Date : 2017-01-01Epub Date: 2017-01-30DOI: 10.18547/gcb.2017.vol3.iss2.e41
Kirti Prakash, David Fournier
Histone modifications alone or in combination are thought to modulate chromatin structure and function; a concept termed histone code. By combining evidence from several studies, we investigated if the histone code can play a role in higher-order folding of chromatin. Firstly using genomic data, we analyzed associations between histone modifications at the nucleosome level. We could dissect the composition of individual nucleosomes into five predicted clusters of histone modifications. Secondly, by assembling the raw reads of histone modifications at various length scales, we noticed that the histone mark relationships that exist at nucleosome level tend to be maintained at the higher orders of chromatin folding. Recently, a high-resolution imaging study showed that histone marks belonging to three of the five predicted clusters show structurally distinct and anti-correlated chromatin domains at the level of chromosomes. This made us think that the histone code can have a significant impact in the overall compaction of DNA: at the level of nucleosomes, at the level of genes, and finally at the level of chromosomes. As a result, in this article, we put forward a theory where the histone code drives not only the functionality but also the higher-order folding and compaction of chromatin.
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Histone modifications alone or in combination are thought to modulate chromatin structure and function; a concept termed histone code. By combining evidence from several studies, we investigated if the histone code can play a role in higher-order folding of chromatin. Firstly using genomic data, we analyzed associations between histone modifications at the nucleosome level. We could dissect the composition of individual nucleosomes into five predicted clusters of histone modifications. Secondly, by assembling the raw reads of histone modifications at various length scales, we noticed that the histone mark relationships that exist at nucleosome level tend to be maintained at the higher orders of chromatin folding. Recently, a high-resolution imaging study showed that histone marks belonging to three of the five predicted clusters show structurally distinct and anti-correlated chromatin domains at the level of chromosomes. This made us think that the histone code can have a significant impact in the overall compaction of DNA: at the level of nucleosomes, at the level of genes, and finally at the level of chromosomes. As a result, in this article, we put forward a theory where the histone code drives not only the functionality but also the higher-order folding and compaction of chromatin.
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