arXiv subjects

Daniel Rico

Publications and source records attributed to Daniel Rico.

3 recordsLinked to original sources

arXiv2024

An entropic analisis of social demonstrations

Social media has dramatically influenced how individuals and groups express their demands, concerns and aspirations during social demonstrations. The study of X or Twitter hashtags during those events has revealed the presence of some temporal points characterised by high correlation among their participants. It has also been reported that the connectivity presents a modular-to-nested transition at the point of maximum correlation. The present study aims to determine whether it is possible to characterise this transition using entropic-based tools. Our results show that entropic analysis can effectively find the transition point to the nested structure, allowing researchers to know that the transition occurs without the need for a network representation. The entropic analysis also shows that the modular-to-nested transition is characterised not by the diversity in the number of hashtags users post but by how many hashtags they share.

physics.soc-ph↗

arXiv2015

Integrating epigenomic data and 3D genomic structure with a new measure of chromatin assortativity

Network analysis is a powerful way of modeling chromatin interactions. Assortativity is a network property used in social sciences to identify factors affecting how people establish social ties. We propose a new approach, using chromatin assortativity to integrate the epigenomic landscape of a specific cell type with its chromatin interaction network and thus investigate which proteins or chromatin marks mediate genomic contacts. We use high-resolution Promoter Capture Hi-C and Hi-Cap data as well as ChIA-PET data from mouse embryonic stem cells to investigate promoter-centered chromatin interaction networks and calculate the presence of specific epigenomic features in the chromatin fragments constituting the nodes of the network. We estimate the association of these features to the topology of four chromatin interaction networks and identify features localized in connected areas of the network. Polycomb Group proteins and associated histone marks are the features with the highest chromatin assortativity in promoter-centred networks. We then ask which features distinguish contacts amongst promoters from contacts between promoters and other genomic elements. We observe higher chromatin assortativity of the actively elongating form of RNA Polymerase 2 (RNAPII) compared to inactive forms only in interactions between promoters and other elements. Contacts among promoters, and between promoters and other elements have different characteristic epigenomic features. We identify a possible role for the elongating form of RNAPII in mediating interactions among promoters, enhancers and transcribed gene bodies. Our approach facilitates the study of multiple genome-wide epigenomic profiles, considering network topology and allowing the comparison of chromatin interaction networks.

q-bio.MN↗

arXiv2013

Late-replicating CNVs as a source of new genes

Asynchronous replication of the genome has been associated with different rates of point mutation and copy number variation (CNV) in human populations. Here, we explored if the bias in the generation of CNV that is associated to DNA replication timing might have conditioned the birth of new protein-coding genes during evolution. We show that genes that were duplicated during primate evolution are more commonly found among the human genes located in late-replicating CNV regions. We traced the relationship between replication timing and the evolutionary age of duplicated genes. Strikingly, we found that there is a significant enrichment of evolutionary younger duplicates in late replicating regions of the human and mouse genome. Indeed, the presence of duplicates in late replicating regions gradually decreases as the evolutionary time since duplication extends. Our results suggest that the accumulation of recent duplications in late replicating CNV regions is an active process influencing genome evolution.

q-bio.GN↗