bioRxiv Science⌕ Search

Biology subjects

Almeida, B.

Publications and source records attributed to Almeida, B..

4 recordsLinked to original sources

Positive supercoiling buildup is a trigger of E. coli's short-term response to cold shock

Adaptation to cold shock (CS) is a key survival skill of gut bacteria of warm-blooded animals. In E. coli, this skill emerges from a complex transcriptional program of multiple, timely-ordered shifts in gene expression. We identified short-term, cold shock repressed (CSR) genes by RNA-seq and provide evidence that their variability in evolutionary fitness is low and that their responsiveness to cold emanates from intrinsic features. Given that their single-cell variability in protein numbers increases after CS, we hypothesized that the responsiveness of a large portion of CSR genes is triggered by the high propensity for transcription locking due to positive supercoiling buildup (PSB). We then proposed a model of this phenomenon and, in support, show that nearly half of CSR genes are highly responsive to Gyrase inhibition. Also, their response strengths to CS and Gyrase inhibition correlate and most CSR genes increase their single-cell variability in protein numbers. Further, during CS, the cells nucleoid density increases (in agreement with increased numbers of positive supercoils), their energy levels become depleted (while the resolving of positive supercoils is ATP dependent), and the colocalization of Gyrases and the nucleoid increases (in agreement with increased time length for resolving supercoils). We conclude that high sensitivity to PSB is at the core of the short-term, cold shock responsive transcriptional program of E. coli and propose that this gene feature may be useful for providing temperature sensitivity to chromosome-integrated synthetic circuits.

systems biology↗

Water yield modelling, sensitivity analysis and validation: a study for Portugal

The spatially explicit assessment of freshwater is key to introduce the ecosystem service (ES) concept into decision-making processes. Many tools are being developed to model water balance and to analyse the effects of meteorological conditions on water ES behaviours at multiple spatial scales. Nevertheless, there is a lack of studies that analyse the sensitivity of these models and estimate the models accuracy. The current research uses the InVEST Water Yield Model (WYM) to assess freshwater ES between 1990 and 2018 at River Basin District (RBD) level in mainland Portugal. The methodology included sensitivity analysis simulations to test different parameters of the model over two different sources of meteorological data. We validated the model with the European Environment Agency (EEA) database on the quantity of Europes freshwater resources. To evaluate the models sensitivity, Pearsons correlation coefficients and statistical methods were calculated for each simulation. The model which obtained the best performance in the sensitivity tests was retained for further analysis and calibration and its accuracy was assessed by comparing the mean estimated water yield (WY) with mean observed values for 2018. Results at the national level show a correlation coefficient of 0.803 with statistical significance for 0.01 one-tail. The WY in the RBDs of the North of the country was underestimated by 56.5 mm/ha/year and for the RBDs in the South of Portugal, the WY was overestimated by 58.1 mm/ha/year. This difference was explained through the spatial-temporal assessment of the main climatic variables used as input. This study contributes to a methodology to assess the level of confidence in WYM outputs and can be used to support the trustworthiness of water availability studies at sub-watershed, watershed, or RBD, using open access data and software.

ecology↗

Targeted cancer therapy induces APOBEC fuelling the evolution of drug resistance

Introductory paragraphThe clinical success of targeted cancer therapy is limited by drug resistance that renders cancers lethal in patients1-4. Human tumours can evolve therapy resistance by acquiring de novo genetic alterations and increased heterogeneity via mechanisms that remain incompletely understood1. Here, through parallel analysis of human clinical samples, tumour xenograft and cell line models and murine model systems, we uncover an unanticipated mechanism of therapy-induced adaptation that fuels the evolution of drug resistance. Targeted therapy directed against EGFR and ALK oncoproteins in lung cancer induced adaptations favoring apolipoprotein B mRNA-editing enzyme, catalytic polypeptide (APOBEC)-mediated genome mutagenesis. In human oncogenic EGFR-driven and ALK-driven lung cancers and preclinical models, EGFR or ALK inhibitor treatment induced the expression and DNA mutagenic activity of APOBEC3B via therapy-mediated activation of NF-{kappa}B signaling. Moreover, targeted therapy also mediated downregulation of certain DNA repair enzymes such as UNG2, which normally counteracts APOBEC-catalyzed DNA deamination events. In mutant EGFR-driven lung cancer mouse models, APOBEC3B was detrimental to tumour initiation and yet advantageous to tumour progression during EGFR targeted therapy, consistent with TRACERx data demonstrating subclonal enrichment of APOBEC-mediated mutagenesis. This study reveals how cancers adapt and drive genetic diversity in response to targeted therapy and identifies APOBEC deaminases as future targets for eliciting more durable clinical benefit to targeted cancer therapy.

cancer biology↗

Regulation of neuronal mRNA splicing and Tau isoform ratio by ATXN3 through deubiquitylation of splicing factors

The ubiquitylation/deubiquitylation balance in cells is maintained by deubiquitylating enzymes, including ATXN3. The precise role of this protein, mutated in spinocerebellar ataxia type 3 (SCA3), remains elusive, as few substrates for its deubiquitylating activity were identified. Here, we characterized the ubiquitome of neuronal cells lacking ATXN3, and found altered polyubiquitylation in a large proportion of proteins involved in RNA metabolism, including splicing factors. Using transcriptomic analysis and reporter minigenes we confirmed that splicing was globally altered in these cells. Among the candidate targets of ATXN3 was SRSF7 (9G8), a key regulator of MAPT (Tau) exon 10 splicing. Loss-of-function of ATXN3 led to reduced SRSF7 levels and a deregulation of MAPT exon 10 splicing, resulting in a decreased 4R/3R-Tau ratio. Similar alterations were found in cellular models of expanded polyQ ATXN3 and SCA3 patient brains, pointing to a relevant role of this mechanism in SCA3, and establishing a previously unsuspected link between two key proteins involved in different neurodegenerative disorders.

neuroscience↗