Biology subjects

Rodriguez, R.

Publications and source records attributed to Rodriguez, R..

4 recordsLinked to original sources

bioRxiv2019

VARIATIONS IN THE COVERAGE OF BIOLOGICAL SOIL CRUSTS ALONG A GRADIENT OF ARIDITY IN THE CENTER-WEST OF ARGENTINA

The biological soil crusts (biocrust) play a fundamental role in the arid and semiarid areas of South America. However, little attention has been paid to the distribution and coverage of them. In Argentina, studies about biocrust are still scarce. The goal of this contribution is to analyze the coverage of the biocrust and each of the functional component along a gradient of aridity in the center-west of Argentina. The gradient included three differentiated sites: semiarid, arid, and hyperarid sites. The coverage was recorded using the Point-quadrat method on 30 transects through a gradient consisting of three sites: semiarid, arid, and hyper-arid sites. The arid site was the system with the highest coverage of biocrust followed by the hyper-arid site. The semiarid site had the lowest values of coverage and showed significant differences among the three systems were found. Cyanobacterias dominate in the hyper-arid site. On the other hand, cyanobacteria and lichens were dominant in the arid site. The coverage of studied organisms showed variations in the semiarid site. These results support the idea that the coverage has a strong relationship with the features of the studied ecosystem and the environmental factors both at a mesoscale and a microscale in a determined community.

ecology↗

bioRxiv2019

CD44 regulates epigenetic plasticity by mediating iron endocytosis

CD44 is a transmembrane glycoprotein that is linked to various biological processes reliant on the epigenetic plasticity of cells, including development, inflammation, immune responses, wound healing and cancer progression. While thoroughly studied, functional regulatory roles of this so-called cell surface marker remain elusive. Here, we report the discovery that CD44 mediates endocytosis of iron interacting with hyaluronates in tumorigenic cell lines and primary cancer cells. We found that this glycan-mediated iron endocytosis mechanism is enhanced during epithelial-mesenchymal transition, unlike the canonical transferrin-dependent pathway. This transition is further characterized by molecular changes required for iron-catalyzed oxidative demethylation of the repressive histone mark H3K9me2 that governs the expression of mesenchymal genes. CD44 itself is transcriptionally regulated by nuclear iron, demonstrating a positive feedback loop, which is in contrast to the negative regulation of transferrin receptor by excess iron. Finally, we show that epigenetic plasticity can be altered by interfering with iron homeostasis using small molecules. This comprehensive study reveals an alternative iron uptake mechanism that prevails in the mesenchymal state of mammalian cells, illuminating a central role of iron as a rate-limiting regulator of epigenetic plasticity.

cell biology↗

bioRxiv2019

Establishment of primary transgenic human airway epithelial cell cultures to study respiratory virus-host interactions

Primary human airway epithelial cell (hAEC) cultures represent a universal platform to propagate respiratory viruses and characterize their host interactions in authentic target cells. To further elucidate specific interactions between human respiratory viruses and important host factors in airway epithelium, it is important to make hAEC cultures amenable to genetic modification. However, the short and finite lifespan of primary cells in cell culture creates a bottleneck for the genetic modification of these cultures. In the current study, we show that the incorporation of the Rho-associated protein kinase (ROCK) inhibitor (Y-27632) during cell propagation extends the life span of primary human cells in vitro and thereby facilitates the incorporation of lentivirus-based expression systems. Using fluorescent reporters for FACS-based sorting, we generated homogenously fluorescent hAEC cultures that differentiate normally after lentiviral transduction. As proof-of-principle, we demonstrate that host gene expression can be modulated post-differentiation via inducible short hairpin (sh)RNA-mediated knockdown. Importantly, functional characterization of these transgenic hAEC cultures with exogenous poly(I:C), as a proxy for virus infection, demonstrates that such modifications do not influence the host innate immune response. Moreover, the propagation kinetics of both human coronavirus 229E (HCoV-229E) and human respiratory syncytial virus (RSV) were not affected. Combined, these results validate our newly established protocol for the genetic modification of hAEC cultures thereby unlocking a unique potential for detailed molecular characterization of virus - host interactions in human respiratory epithelium.

microbiology↗

bioRxiv2019

CytoGPS: A Web-Enabled Karyotype Analysis Tool for Cytogenetics

Karyotype data are the most common form of genetic data that is regularly used clinically. They are collected as part of the standard of care in many diseases, particularly in pediatric and cancer medicine contexts. Karyotypes are represented in a unique text-based format, with a syntax defined by the International System for human Cytogenetic Nomenclature (ISCN). While human-readable, ISCN is not intrinsically machine-readable. This limitation has prevented the full use of complex karyotype data in discovery science use cases. To enhance the utility and value of karyotype data, we developed a tool named CytoGPS. CytoGPS first parses ISCN karyotypes into a machine-readable format. It then converts the ISCN karyotype into a binary Loss-Gain-Fusion (LGF) model, which represents all cytogenetic abnormalities as combinations of loss, gain, or fusion events, in a format that is analyzable using modern computational methods. Such data is then made available for comprehensive \"downstream\" analyses that previously were not feasible.\n\nAvailability and ImplementationFreely available at https://cytogps.org\n\nContactprpayne@wustl.edu\n\nSupplementary informationNot applicable

bioinformatics↗