Expression of BRCC3, a novel cell cycle regulated molecule, is associated with increased phospho-ERK and cell proliferation

Boudreau, Howard E.; Broustas, Constantinos G.; Gokhale, Prafulla C.; Kumar, Deepak; Mewani, Rajshree R.; Rone, Janice D.; Haddad, Bassem R.; Kasid, Usha N.

doi:10.3892/ijmm.19.1.29

Cited by 33 publications

(45 citation statements)

References 45 publications

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“…1). These genes were, SET translocation (SET) [15], DEAD (Asp-Glu-Ala-Asp) box polypeptide 1 (Ddx1) [16], COMM domain containing 3 (Commd3) [17] and BRCA1/BRCA2-containing complex, subunit 3 (Brcc3) [18]. SET has been assumed to play a role in nucleosome assembly [15].…”

Section: Resultsmentioning

confidence: 99%

Identification of Genes Differentially Expressed in Mouse Fetuses from Streptozotocin-induced Diabetic Pregnancy by cDNA Subtraction

et al. 2008

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Abstract. Epidemiological studies have shown that the risks of fetal malformation such as neural tube defects increase in diabetic pregnancy. To explore the mechanism of fetal malformation induced by diabetes, cDNA subtraction using mouse embryos (E9.5) of diabetic dams and those of controls was performed to identify differentially expressed genes. The expression level of genes identified by cDNA subtraction was further verified by quantitative RT-PCR using E8.5 embryos, and differential expression of 4 genes, Brcc3, Commd3, Ddx1, and SET was confirmed. We also analyzed the expression level of neural tube defect-related genes, and found that Folbp1, EphrinA5 and Sox10 were differentially expressed. Altered expression of these genes mostly persisted throughout the later stages of the development (E10.5-14.5). Hierarchical clustering analysis showed correlation between expression levels of these genes, suggesting that these genes cooperatively play a role in embryonic development. Our results suggest that an altered gene expression profile in embryos underlies the development of congenital malformation in diabetic pregnancies.

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Section: Resultsmentioning

confidence: 99%

Identification of Genes Differentially Expressed in Mouse Fetuses from Streptozotocin-induced Diabetic Pregnancy by cDNA Subtraction

et al. 2008

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“…Within several of the conserved MIGs identified herein, mutations have been linked to abnormal cell proliferation or cancer in humans. For example, mutations in BRCC3, which encodes a cell cycle regulator involved in G2/M phase transition, has been linked to myelodysplastic syndrome (MDS), as well as breast and cervical cancers (Boudreau et al 2007;Huang et al 2015;Zhang, Zhou 2018). Mutations in E2F3 have been associated with retinoblastoma, bladder and lung cancer (Ziebold et al 2001;Wang et al 2017a;Liu et al 2018).…”

Section: Discussionmentioning

confidence: 99%

Genetic Analysis of Human RNA Binding Motif Protein 48 (RBM48) Reveals an Essential Role in U12-Type Intron Splicing

Siebert

Corll

Gronevelt

et al. 2020

Preprint

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U12-type (minor) introns are found in most multicellular eukaryotes, and constitute ~0.5% of all introns in species with a minor spliceosome required for their splicing. However, the biological relevance of U12-type introns is not well understood. It is known that mutations resulting in aberrant U12-type intron splicing cause developmental defects in both plants and animals. We recently reported that maize RNA Binding Motif Protein 48 (RBM48) is an essential splicing factor for U12-type introns. Maize rbm48 mutants display aberrant genome-wide U12-type intron splicing. This leads to severe defects in endosperm development, resulting in non-viable seeds. In this report, we use CRISPR/Cas9-mediated ablation of RBM48 in human K-562 cells to establish the evolutionary conservation of RBM48 dependent U12-type intron splicing between maize and humans. Comparative RNA-seq analysis performed on RBM48 deficient human cell lines and maize endosperm defined a subset of orthologous minor U12-type containing genes (MIGs) displaying aberrant splicing of U12-type introns in both species. Mutations in the majority of these MIGs have been reported to cause developmental defects in both plants and animals. Thus, a comparison of RNA-seq data between distantly related species containing mutations in RBM48 identifies candidate genes likely to mediate mutant phenotypes of U12-type splicing defects. Our results elucidate deeply conserved post-transcriptional processing mechanisms that are required for normal growth and development of eukaryotes with a minor spliceosome.

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“…Therefore, our findings indicate that regulation of TRIO and DEPDC1B expression by Pitx2 leads to the activation of RAC1 and RHOA, thus contributing to the regulation of cell migration during embryonic development. Although a role for DEPDC1B in the regulation of cell migration during embryonic development remains to be elucidated, studies using cultured cells have demonstrated that DEPDC1B is implicated in the regulation of cell migration and cell proliferation [57-59]. …”

Section: Discussionmentioning

confidence: 99%

Identification of the GTPase-activating protein DEP domain containing 1B (DEPDC1B) as a transcriptional target of Pitx2

Zhu

Jimenez-Cowell

et al. 2015

Experimental Cell Research

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Pitx2 is a bicoid-related homeobox transcription factor implicated in regulating left-right patterning and organogenesis. However, only a limited number of Pitx2 downstream target genes have been identified and characterized. Here we demonstrate that Pitx2 is a transcriptional repressor of DEP domain containing 1B (DEPDC1B). The first intron of the human and mouse DEP domain containing 1B genes contains multiple consensus DNA-binding sites for Pitx2. Chromatin immunoprecipitation assays revealed that Pitx2, along with histone deacetylase 1, was recruited to the first intron of Depdc1b. In contrast, RNAi-mediated depletion of Pitx2 not only enhanced the acetylation of histone H4 in the first intron of Depdc1b, but also increased the protein level of Depdc1b. Luciferase reporter assays also showed that Pitx2 could repress the transcriptional activity mediated by the first intron of human DEPDC1B. The GAP domain of DEPDC1B interacted with nucleotide-bound forms of RAC1 in vitro. In addition, exogenous expression of DEPDC1B suppressed RAC1 activation and interfered with actin polymerization induced by the guanine nucleotide exchange factor TRIO. Moreover, DEPDC1B interacted with various signaling molecules such as U2af2, Erh, and Salm. We propose that Pitx2-mediated repression of Depdc1b expression contributes to the regulation of multiple molecular pathways, such as Rho GTPase signaling.

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Expression of BRCC3, a novel cell cycle regulated molecule, is associated with increased phospho-ERK and cell proliferation

Cited by 33 publications

References 45 publications

Identification of Genes Differentially Expressed in Mouse Fetuses from Streptozotocin-induced Diabetic Pregnancy by cDNA Subtraction

Identification of Genes Differentially Expressed in Mouse Fetuses from Streptozotocin-induced Diabetic Pregnancy by cDNA Subtraction

Genetic Analysis of Human RNA Binding Motif Protein 48 (RBM48) Reveals an Essential Role in U12-Type Intron Splicing

Identification of the GTPase-activating protein DEP domain containing 1B (DEPDC1B) as a transcriptional target of Pitx2

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