Calderón encodes an organic cation transporter of the major facilitator superfamily required for cell growth and proliferation of Drosophila tissues

The adaptation of growth in response to dietary changes is essential for the normal development of all organisms. The insulin receptor (InR) signalling pathway controls growth and metabolism in response to nutrient availability. The elements of this pathway have been described, although little is known about the downstream elements regulated by this cascade. We identified calderón, a gene that encodes a protein with highest homology with organic cation transporters of the major facilitator superfamily, as a new transcriptional target of the InR pathway. These transporters are believed to function mainly in the uptake of sugars, as well as other organic metabolites. Genetic experiments demonstrate that calderón is required cell autonomously and downstream of the InR pathway for normal growth and proliferation of larval tissues. Our results indicate that growth of imaginal cells may be modulated by two distinct, but coordinated, nutrient-sensing mechanisms: one cell-autonomous and the other humoral.Dirección General de Investigación Científica y Técnica (BFU2004-00167/BMC) and by EU research contract LSHM-CP-2003-503330 (APOPIS). Work in G.M.’s laboratory is funded by a grant from the Dirección General de Investigación Científica y Técnica (BMC2002-01959)Peer Reviewe

Yorkie and JNK Control Tumorigenesis in Drosophila Cells with Cytokinesis Failure

Summary: Cytokinesis failure may result in the formation of polyploid cells, and subsequent mitosis can lead to aneuploidy and tumor formation. Tumor suppressor mechanisms limiting the oncogenic potential of these cells have been described. However, the universal applicability of these tumor-suppressive barriers remains controversial. Here, we use Drosophila epithelial cells to investigate the consequences of cytokinesis failure in vivo. We report that cleavage defects trigger the activation of the JNK pathway, leading to downregulation of the inhibitor of apoptosis DIAP1 and programmed cell death. Yorkie overcomes the tumor-suppressive role of JNK and induces neoplasia. Yorkie regulates the cell cycle phosphatase Cdc25/string, which drives tumorigenesis in a context of cytokinesis failure. These results highlight the functional significance of the JNK pathway in epithelial cells with defective cytokinesis and elucidate a mechanism used by emerging tumor cells to bypass this tumor-suppressive barrier and develop into tumors. : Cytokinesis failure can be tumorigenic. Gerlach et al. show that JNK represses the expansion of those cells. Yorkie, the Drosophila ortholog of YAP and effector of the Hippo pathway, is able to bypass this barrier in cells with cytokinesis defects and cause neoplastic tumors. Keywords: cytokinesis failure, Drosophila, CDC25, cancer, JNK, Hippo pathway, cell cycle, genomic instabilit

The chromatin remodeling BAP complex limits tumor-promoting activity of the Hippo pathway effector Yki to prevent neoplastic transformation in Drosophila epithelia

Switch/sucrose non-fermentable (SWI/SNF) chromatin remodeling complexes are mutated in many human cancers. In this article, we make use of a Drosophila genetic model for epithelial tumor formation to explore the tumor suppressive role of SWI/SNF complex proteins. Members of the BAP complex exhibit tumor suppressor activity in tissue overexpressing the Yorkie (Yki) proto-oncogene, but not in tissue overexpressing epidermal growth factor receptor (EGFR). The Brahma-associated protein (BAP) complex has been reported to serve as a Yki-binding cofactor to support Yki target expression. However, we observed that depletion of BAP leads to ectopic expression of Yki targets both autonomously and non-autonomously, suggesting additional indirect effects. We provide evidence that BAP complex depletion causes upregulation of the Wingless (Wg) and Decapentaplegic (Dpp) morphogens to promote tumor formation in cooperation with Yki

El método de elementos finitos en la valoración de opciones

En este trabajo se expone una introducción a los conceptos propios de la teoría de valoración de derivados financieros prestando especial atención a las opciones. Asimismo, se presenta el método de los elementos finitos para la resolución de ecuaciones en derivadas parciales justificando su uso desde el marco teórico. Finalmente, se muestran sendos algoritmos del método en algunos problemas de valoración de derivados financieros.Grado en Matemática

Generation of medial and lateral dorsal body domains by the pannier gene of Drosophila

The pannier (pnr) gene encodes a GATA transcription factor and acts in several developmental processes in Drosophila, including embryonic dorsal closure, specification of cardiac cells and bristle determination. We show that pnr is expressed in the mediodorsal parts of thoracic and abdominal segments of embryos, larvae and adult flies. Its activity confers cells with specific adhesion properties that make them immiscible with non-expressing cells. Thus there are two genetic domains in the dorsal region of each segment: a medial (MED) region where pnr is expressed and a lateral (LAT) region where it is not. The homeobox gene iroquois (iro) is expressed in the LAT region. These regions are not formed by separate polyclones of cells, but are defined topographically. We show that ectopic pnr in the wing induces MED thoracic development, indicating that pnr specifies the identity of the MED regions. Correspondingly, when pnr is removed from clones of cells in the MED domain, they sort out and apparently adopt the LAT fate. We propose that (1) the subdivision into MED and LAT regions is a general feature of the Drosophila body plan and (2) pnr is the principal gene responsible for this subdivision. We argue that pnr acts like a classical selector gene but differs in that its expression is not propagated through cell divisions.Dirección General de Investigación Científica y Técnica and the Fundación Ramón ArecesPeer Reviewe

Synthesis of Gold Nanoparticles and Incorporation to a Porous Nickel Electrode to Improve its Catalytic Performance Towards the Hydrogen Evolution Reaction

[EN] Gold nanoparticles (AuNPs) were successfully synthesized by a facile chemical reduction method in the presence of the stabilizer polyvinylpyrrolidone and characterized by UV-vis spectroscopy and transmission electron microscopy. The gold nanoparticles were then incorporated onto the surface of a porous Ni electrode by simple addition of the nanoparticles suspension, followed by heat treatment at 350 degrees C for 1 h under nitrogen atmosphere. The modified electrode was morphologically characterized by field emission scanning electron microscopy. Then, the effect of the modification with Au nanoparticles was studied in the hydrogen evolution reaction (HER) by pseudo-steady-state polarization curves and electrochemical impedance spectroscopy (EIS), at different temperatures and compared with a pure porous Ni electrode. The modified electrode showed a clear improvement in its catalytic performance mainly due to the intrinsic catalytic activity of the Au nanoparticles. From the Tafel representations and the EIS, it was estimated that the HER on the electrode modified with AuNPs takes place by the Volmer-Heyrovsky mechanism.Ramiro Medina Orta is grateful to Consejo Nacional Ciencia y Tecnologia and Consejo Potosino de Ciencia y Tecnologia for the doctorate scholarship 472041. Also, he wishes to thank the Instituto de Metalurgia of Universidad Autonoma de San Luis Potosi for the opportunity of a research stay. We also thank Dr. Nubia Arteaga Larios and M.M.I.M. Martha Alejandra Lomeli Pacheco (Instituto de Metalurgia, Universidad Autonoma de San Luis Potosi) for their help with the UV-vis spectroscopy.Medina-Orta, R.; Labrada-Delgado, GJ.; Silva-Pereyra, HG.; Ortega Navarro, EM.; Pérez-Herranz, V.; Sánchez-Loredo, MG. (2022). Synthesis of Gold Nanoparticles and Incorporation to a Porous Nickel Electrode to Improve its Catalytic Performance Towards the Hydrogen Evolution Reaction. Electrocatalysis. 13(1):47-61. https://doi.org/10.1007/s12678-021-00690-7476113