Drosophila DAxud1 Has a Repressive Transcription Activity on Hsp70 and Other Heat Shock Genes

DAxud1 is a transcription factor that belongs to the Cysteine Serine Rich Nuclear Protein (CSRNP) family, conserved in metazoans, with a transcriptional transactivation activity. According to previous studies, this protein promotes apoptosis and Wnt signaling-mediated neural crest differentiation in...

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Published inInternational journal of molecular sciences Vol. 24; no. 8; p. 7485
Main Authors Zuñiga-Hernandez, Jorge, Meneses, Claudio, Bastias, Macarena, Allende, Miguel L, Glavic, Alvaro
Format Journal Article
LanguageEnglish
Published Switzerland MDPI 19.04.2023
MDPI AG
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Summary:DAxud1 is a transcription factor that belongs to the Cysteine Serine Rich Nuclear Protein (CSRNP) family, conserved in metazoans, with a transcriptional transactivation activity. According to previous studies, this protein promotes apoptosis and Wnt signaling-mediated neural crest differentiation in vertebrates. However, no analysis has been conducted to determine what other genes it might control, especially in connection with cell survival and apoptosis. To partly answer this question, this work analyzes the role of DAxud1 using Targeted-DamID-seq (TaDa-seq), which allows whole genome screening to determine in which regions it is most frequently found. This analysis confirmed the presence of DAxud1 in groups of pro-apoptotic and Wnt pathway genes, as previously described; furthermore, stress resistance genes that coding heat shock protein (HSP) family genes were found as , , and . The enrichment of DAxud1 also identified a DNA-binding motif (AYATACATAYATA) that is frequently found in the promoters of these genes. Surprisingly, the following analyses demonstrated that DAxud1 exerts a repressive role on these genes, which are necessary for cell survival. This is coupled with the pro-apoptotic and cell cycle arrest roles of DAxud1, in which repression of complements the maintenance of tissue homeostasis through cell survival modulation.
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ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms24087485