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The Drosophila kikkawai feature with NCBI Gene ID 108084518 was determined to be an ortholog of Drosophila melanogaster Sox102F, a member of the FlyBase High Mobility Group Box Transcription Factors gene group (FBgg0000748). Five isoforms were constructed using the GEP F element annotation protocol, the longest being novel isoform Sox102F-PNE (identified using the XM_017180752 RefSeq prediction and RNA-seq data). Among the isoforms found in both D. melanogaster and D. kikkawai, Sox102F-PB is the longest and exhibits a 1.18x coding span expansion due to transposable element insertion into an intron. All D. kikkawai protein isoforms contain the conserved domain HMG_box_dom (IPR009071).
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Gene model for the ortholog of Myc in Drosophila eugracilis
Gene model for the ortholog of Myc (Myc) in the D. eugracilis Apr. 2013 (BCM-HGSC/Deug_2.0) (DeugGB2) Genome Assembly (GenBank Accession: GCA_000236325.2) of Drosophila eugracilis. This ortholog was characterized as part of a developing dataset to study the evolution of the Insulin/insulin-like growth factor signaling pathway (IIS) across the genus Drosophila using the Genomics Education Partnership gene annotation protocol for Course-based Undergraduate Research Experiences.
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- Award ID(s):
- 1915544
- PAR ID:
- 10545629
- Publisher / Repository:
- microPublication Biology
- Date Published:
- Format(s):
- Medium: X
- Sponsoring Org:
- National Science Foundation
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The Drosophila kikkawai feature with Gene ID 108083276 was determined to be an ortholog of Drosophila melanogaster absent, small, or homeotic discs 1 (ash1). Two isoforms, ash1-PB and ash1-PC, were constructed on the D. kikkawai Muller D element using the GEP annotation protocol. The second coding exon of D. kikkawai ash1 includes an insertion translated into 18 additional amino acids compared to the D. melanogaster protein and is supported by RNA-Seq coverage, the lack of splice junction predictions, and multiple gene predictors. The first intron in both isoforms of D. kikkawai ash1 contains a well conserved non-canonical GC splice site.more » « less
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Abstract How a developing organ robustly coordinates the cellular mechanics and growth to reach a final size and shape remains poorly understood. Through iterations between experiments and model simulations that include a mechanistic description of interkinetic nuclear migration, we show that the local curvature, height, and nuclear positioning of cells in theDrosophilawing imaginal disc are defined by the concurrent patterning of actomyosin contractility, cell-ECM adhesion, ECM stiffness, and interfacial membrane tension. We show that increasing cell proliferation via different growth-promoting pathways results in two distinct phenotypes. Triggering proliferation through insulin signaling increases basal curvature, but an increase in growth through Dpp signaling and Myc causes tissue flattening. These distinct phenotypic outcomes arise from differences in how each growth pathway regulates the cellular cytoskeleton, including contractility and cell-ECM adhesion. The coupled regulation of proliferation and cytoskeletal regulators is a general strategy to meet the multiple context-dependent criteria defining tissue morphogenesis.more » « less
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Abstract BackgroundSome marine invertebrate organisms are considered not to develop tumors due to unknown mechanisms. To gain an initial insight into how tumor‐related genes may be expressed and function during marine invertebrate development, we here leverage sea urchin embryos as a model system and characterize the expressions of Myc and p53/p63/p73 which are reported to function synergistically in mammalian models as an oncogene and tumor suppressor, respectively. ResultsDuring sea urchin embryogenesis, a combo gene of p53/p63/p73 is found to be maternally loaded and decrease after fertilization both in transcript and protein, while Myc transcript and protein are zygotically expressed. p53/p63/p73 and Myc proteins are observed in the cytoplasm and nucleus of every blastomere, respectively, throughout embryogenesis. Both p53/p63/p73 and Myc overexpression results in compromised development with increased DNA damage after the blastula stage. p53/p63/p73 increases the expression ofparp1, a DNA repair/cell death marker gene, and suppresses endomesoderm gene expressions. In contrast, Myc does not alter the expression of specification genes or oncogenes yet induces disorganized morphology. Conclusionsp53/p63/p73 appears to be important for controlling cell differentiation, while Myc induces disorganized morphology yet not through conventional oncogene regulations or apoptotic pathways during embryogenesis of the sea urchin.more » « less
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The MYC oncogenic transcription factor is acetylated by the p300 and GCN5 histone acetyltransferases. The significance of MYC acetylation and the functions of specific acetylated lysine (AcK) residues have remained unclear. Here, we show that the major p300-acetylated K148(149) and K157(158) sites in human (or mouse) MYC and the main GCN5-acetylated K323 residue are reversibly acetylated in various malignant and nonmalignant cells. Oncogenic overexpression of MYC enhances its acetylation and alters the regulation of site-specific acetylation by proteasome and deacetylase inhibitors. Acetylation of MYC at different K residues differentially affects its stability in a cell type-dependent manner. Lysine-to-arginine substitutions indicate that although none of the AcK residues is required for MYC stimulation of adherent cell proliferation, individual AcK sites have gene-specific functions controlling select MYC-regulated processes in cell adhesion, contact inhibition, apoptosis, and/or metabolism and are required for the malignant cell transformation activity of MYC. Each AcK site is required for anchorage-independent growth of MYC-overexpressing cells in vitro, and both the AcK148(149) and AcK157(158) residues are also important for the tumorigenic activity of MYC transformed cells in vivo. The MYC AcK site-specific signaling pathways identified may offer new avenues for selective therapeutic targeting of MYC oncogenic activities.more » « less
- Free Publicly Accessible Full Text
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Accepted Manuscript1.0
- Data Paper:
- https://doi.org/10.17912/micropub.biology.000912
