TY - JOUR AU - Haddadi, Mohammad AU - Ataei, Reza TI - wde, calpA, if, dap160, and poe genes knock down Drosophila models exhibit neurofunctional deficit JF - GENE J2 - GENE VL - 829 PY - 2022 PG - 11 SN - 0378-1119 DO - 10.1016/j.gene.2022.146499 UR - https://m2.mtmt.hu/api/publication/32977032 ID - 32977032 AB - Intellectual disability (ID) is a heterogeneous disorder with high prevalence and remarkable social and cost burdens. Novel genetic variants of ATF7IP, CAPN9, ITGAV, ITSN1, and UBR4 genes are reported to be associated with the ID among Iranian families. However, in vivo validation is required to confirm the functional role of these variants in ID development. Drosophila melanogaster is a convenient model for such functional investigations as its genome bears ortholog of more than 75% of the disease-causing genes in human and represents numerous approaches to study defects in neuronal function. In this connection, RNAi gene silencing was applied to wde, calpA, if, dap160, and poe genes, the Drosophila ortholog of the selected human genes, and then consequent structural and functional changes in neurons were studied by means of immunohistochemistry and confocal microscopy of mushroom bodies (MBs) and validated behavioural assays including larvae and adult conditioning learning and memories, and ethanol sensitivity. Down-regulation of these genes led to neuronal loss which was evident by decline in total fluorescent signal intensity in micrographs of MBs structure. The gene silencing caused neuronal dysfunction and induction of ID-like symptoms manifested by deficits in larval preference learning, and shortterm olfactory memory and courtship suppression learning in adults. Moreover, the RNAi flies showed higher sensitivity to ethanol vapour. Interestingly, the poe knock-down flies exhibited the most severe phenotypes among other genes. Altogether, we believe this study is first-of-its-kind and findings are highly applicable to confirm pathogenecity of the selected ID gene variants in Iranian population. LA - English DB - MTMT ER - TY - JOUR AU - Araujo, H. AU - Julio, A. AU - Cardoso, M. TI - Translating genetic, biochemical and structural information to the calpain view of development JF - MECHANISMS OF DEVELOPMENT J2 - MECH DEVELOP VL - 154 PY - 2018 SP - 240 EP - 250 PG - 11 SN - 0925-4773 DO - 10.1016/j.mod.2018.07.011 UR - https://m2.mtmt.hu/api/publication/30378948 ID - 30378948 N1 - Export Date: 8 January 2019 CODEN: MEDVE Correspondence Address: Araujo, H.; Institute for Biomedical Sciences, Federal University of Rio de Janeiro, Av. Carlos Chagas Filho, 373, Bloco F – Sala F2-031, Brazil; email: haraujo@histo.ufrj.br Chemicals/CAS: calcium, 7440-70-2, 14092-94-5; calpain, 78990-62-2; calpain 1; calpain 2, 702693-80-9; calpain 3 Funding details: Conselho Nacional de Desenvolvimento Científico e Tecnológico, CNPq Funding details: Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro, FAPERJ Funding text 1: This work was supported by funds from FAPERJ /Brazil to HA and CNPq fellowships to MC and AJ. We thank the Araujo lab for helpful comments on the manuscript. Cited By :5 Export Date: 12 May 2021 CODEN: MEDVE Correspondence Address: Araujo, H.; Institute for Biomedical Sciences, Av. Carlos Chagas Filho, 373, Bloco F – Sala F2-031, Brazil; email: haraujo@histo.ufrj.br Chemicals/CAS: calcium, 7440-70-2, 14092-94-5; calpain, 78990-62-2; calpain 1; calpain 2, 702693-80-9; calpain 3; protein, 67254-75-5; Calpain; Proteins Funding details: Conselho Nacional de Desenvolvimento Científico e Tecnológico, CNPq Funding details: Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro, FAPERJ Funding text 1: This work was supported by funds from FAPERJ /Brazil to HA and CNPq fellowships to MC and AJ. We thank the Araujo lab for helpful comments on the manuscript. Funding text 2: This work was supported by funds from FAPERJ/Brazil to HA and CNPq fellowships to MC and AJ. We thank the Araujo lab for helpful comments on the manuscript. Funding Agency and Grant Number: FAPERJ/BrazilFundacao Carlos Chagas Filho de Amparo a Pesquisa do Estado do Rio De Janeiro (FAPERJ); CNPqConselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPQ) Funding text: This work was supported by funds from FAPERJ/Brazil to HA and CNPq fellowships to MC and AJ. We thank the Araujo lab for helpful comments on the manuscript. AB - Embryonic development repeatedly deploys a finite number of signaling pathways to control a multitude of processes such as patterning, growth and differentiation. Diversity in gene expression resulting from these signals depends on the epigenetic landscape as well as the network of interactions between different pathways at a given time. A third mechanism to generate diversity from a sole signal is to modify downstream pathway effectors by modulatory protein activity. The calcium-dependent calpain proteases are modulatory proteases that cleave proteins at specific sites, generating fragments, or neoproteins, with novel functions. Among calpain substrates are effectors of the Wnt and NFκB pathways, ERK pathway and ionic channel receptors, and cell cycle regulators. Loss of calpain function is associated to muscular dystrophy, deterioration of neural connections and embryonic patterning defects. Here we review the basic features of calpains, the principles that guide regulation by calpain activity, and recent literature on how calpain function controls fundamental aspects of animal development. © 2018 Elsevier B.V. LA - English DB - MTMT ER - TY - JOUR AU - Bilak, A AU - Uyetake, L AU - Su, TT TI - Dying Cells Protect Survivors from Radiation-Induced Cell Death in Drosophila JF - PLOS GENETICS J2 - PLOS GENET VL - 10 PY - 2014 IS - 3 SN - 1553-7390 DO - 10.1371/journal.pgen.1004220 UR - https://m2.mtmt.hu/api/publication/24102005 ID - 24102005 LA - English DB - MTMT ER - TY - JOUR AU - Fontenele, Marcio AU - Lim, Bomyi AU - Oliveira, Danielle AU - Buffolo, Marcio AU - Perlman, David H AU - Schupbach, Trudi AU - Araujo, Helena TI - Calpain A modulates Toll responses by limited Cactus/I kappa B proteolysis JF - MOLECULAR BIOLOGY OF THE CELL J2 - MOL BIOL CELL VL - 24 PY - 2013 IS - 18 SP - 2966 EP - 2980 PG - 15 SN - 1059-1524 DO - 10.1091/mbc.E13-02-0113 UR - https://m2.mtmt.hu/api/publication/24777190 ID - 24777190 N1 - Megjegyzés-24212710 N1 Funding Details: HHMI, Howard Hughes Medical Institute Megjegyzés-26256829 N1 Funding details: HHMI, Howard Hughes Medical Institute Megjegyzés-23369860 N1 Funding Details: HHMI, Howard Hughes Medical Institute LA - English DB - MTMT ER -