About the Teaching and Learning of Differentiability for Piecewise Functions in Science Degrees’ First-Year Calculus Courses

In this work, we present an issue we have observed over the last several years in the first year of Spanish science degrees’ (such as mathematics, physics or engineering) calculus courses. It is related to the study of differentiability of piecewise one real variable real functions at a point. We have analyzed how students study the differentiability of piecewise functions at a point, explaining the students’ work and reasoning and commenting about the common misunderstandings we have found. Then, we have researched about how to help the students in their learning process related to this calculus concept, and we have also used several activities or ways to work: student meeting groups to talk about their worries and misunderstandings, mathematical definitions, explanations and theory and also working out specific examples

Alan Turing-ek morfogenesiaren inguruan egindako ikerketaren analisi matematikoa

Artikulu honetan, Alan Turing matematikariak 1952an morfogenesiaren inguruan aurkeztu zuen The Chemical Basis of Morphogenesis, [19], lanaren zati bat aurkeztu eta matematikoki garatuko dugu. Horretarako, beharrezkoak diren matematikako kontzeptuak eta baliabideak azalduko ditugu. Konkretuki, Alan Turingek [19] artikuluko "Reactions and Diffusion in a Ring of Cells" (eraztun diskretuko eremua) eta "Continuous Ring of Tissue" (eraztun jarraituko eremua) ataletan gehiegi sakondu edo zehaztu gabe erabili zituen ekuazio diferentzialak, erreakzio-difusio ekuazioak, Fourieren serieak eta funtzioen linealizazioa azalduko ditugu, eta bi eremu horietan planteatutako ekuazio-sistemen soluzioak bilatzeko erabiliko ditugu. Artikulu hau UPV/EHUko Idoia Marauri ikasle ohiaren Gradu Amaierako Lanean oinarrituta dago.; In this article, we show and mathematically develop a part of the work that the mathematician Alan Turing did on Morphogenesis which he published in 1952 in his article The Chemical Basis of Morphogenesis. We will explain the mathematical concepts and resources needed to do so: differential equations, reaction-diffusion equations, Fourier series and function linearization. Specifically, we will show and explain all these mathematical tools that Alan Turing used but did not develop nor delve into a lot in his aforementioned article’s two sections: “Reactions and Diffusion in a Ring of Cells" (for the discrete ring region) and “Continuous Ring of Tissue" (for the continuous ring region). This article is based on the UPV/EHU former student Idoia Marauri’s Final Degree Project

E2F7 regulates transcription and maturation of multiple microRNAs to restrain cell proliferation

This work was supported by the Spanish Ministry [SAF2012-33551, co-funded by the European RegionalDevelopment fund to A.M.Z., SAF2012-38215 to M.M.,SAF2014-57791-REDC to A.M.Z. and to M.M.]; BasqueGovernment [IT634-13 to A.M.Z.]; University of theBasque Country UPV/EHU [UFI1120 to A.M.Z.]; Excellence Network CellSYS [BFU2014-52125-REDT to M.M.];Comunidad de Madrid [S2010/BMD-2470 to M.M.];Basque Government Fellowship for graduate studies (to J.M.). Funding for open access charge: Basque Government [IT634-13]. Conflict of interest statement. None declared.E2F transcription factors (E2F1-8) are known to coordinately regulate the expression of a plethora of target genes, including those coding for microRNAs (miRNAs), to control cell cycle progression. Recent work has described the atypical E2F factor E2F7 as a transcriptional repressor of cell cycle-related protein-coding genes. However, the contribution of E2F7 to miRNA gene expression during the cell cycle has not been defined. We have performed a genome-wide RNA sequencing analysis to identify E2F7-regulated miRNAs and show that E2F7 plays as a major role in the negative regulation of a set of miRNAs that promote cellular proliferation. We provide mechanistic evidence for an interplay between E2F7 and the canonical E2F factors E2F1-3 in the regulation of multiple miRNAs. We show that miR-25, -26a, -27b, -92a and -7 expression is controlled at the transcriptional level by the antagonistic activity of E2F7 and E2F1-3. By contrast, let-7 miRNA expression is controlled indirectly through a novel E2F/c-MYC/LIN28B axis, whereby E2F7 and E2F1-3 modulate c-MYC and LIN28B levels to impact let-7 miRNA processing and maturation. Taken together, our data uncover a new regulatory network involving transcriptional and post-transcriptional mechanisms controlled by E2F7 to restrain cell cycle progression through repression of proliferation-promoting miRNAs.S

An E2F7-Dependent Transcriptional Program Modulates DNA Damage Repair And Genomic Stability

Corrigendum published on 03 July 2019 Nucleic Acids Research 47 (14) : 7716–7717 (2019) https://doi.org/10.1093/nar/gkz587The cellular response to DNA damage is essential for maintaining the integrity of the genome. Recent evidence has identified E2F7 as a key player in DNA damage-dependent transcriptional regulation of cell-cycle genes. However, the contribution of E2F7 to cellular responses upon genotoxic damage is still poorly defined. Here we show that E2F7 represses the expression of genes involved in the maintenance of genomic stability, both throughout the cell cycle and upon induction of DNA lesions that interfere with replication fork progression. Knockdown of E2F7 leads to a reduction in 53BP1 and FANCD2 foci and to fewer chromosomal aberrations following treatment with agents that cause interstrand crosslink (ICL) lesions but not upon ionizing radiation. Accordingly, E2F7-depleted cells exhibit enhanced cell-cycle re-entry and clonogenic survival after exposure to ICL-inducing agents. We further report that expression and functional activity of E2F7 are p53-independent in this context. Using a cell-based assay, we show that E2F7 restricts homologous recombination through the transcriptional repression of RAD51. Finally, we present evidence that downregulation of E2F7 confers an increased resistance to chemotherapy in recombination-deficient cells. Taken together, our results reveal an E2F7-dependent transcriptional program that contributes to the regulation of DNA repair and genomic integrity.This work was supported by grants from the Spanish Ministry [SAF2012-33551 and SAF2015-67562-R, co-financed by FEDER funds, and SAF2014-57791-REDC], the Basque Government [IT634-13 and KK-2015/89], and the University of the Basque Country UPV/EHU [UFI11/20] to AMZ; and grants from the Spanish Ministry [SAF2015-69920-R], and Worldwide Cancer Research [15-0278] to MM. JM was recipient of a Basque Government fellowship for graduate studies and JVR is recipient of a UPV/EHU fellowship for graduate studies. M.A.F. was supported by a young investigator grant from MINECO [SAF2014-60442-JIN; co-financed by FEDER funds]. Funding for open access charge: Spanish Ministry [SAF2015-67562-R, co-financed by FEDER funds]; Basque Government [IT634-13]