Yeast two‐hybrid screens imply that GGNBP1, GGNBP2 and OAZ3 are potential interaction partners of testicular germ cell‐specific protein GGN1

Zhang, Jin; Yan, Wei; Zhou, Yu; Chen, Zhiguo; Huang, Peitang; Lü, Biao

doi:10.1016/j.febslet.2004.10.112

Cited by 48 publications

(46 citation statements)

References 29 publications

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“…It has been reported that GGNBP2 interacts with testicular proteins, GGN1, GGNBP1, CRISP2 and OAZ3 26, 28, 29, 30. Reciprocal immunoprecipitation (IP) with GGN (Figure 3A) and GGNBP2 (Figure 3B) antibodies demonstrated that GGN1 and GGNBP2 formed a protein complex in the testis.…”

Section: Resultsmentioning

confidence: 86%

Ablation of Ggnbp2 impairs meiotic DNA double‐strand break repair during spermatogenesis in mice

Guo

Liu

et al. 2018

J Cellular Molecular Medi

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Gametogenetin (GGN) binding protein 2 (GGNBP2) is a zinc finger protein expressed abundantly in spermatocytes and spermatids. We previously discovered that Ggnbp2 resection caused metamorphotic defects during spermatid differentiation and resulted in an absence of mature spermatozoa in mice. However, whether GGNBP2 affects meiotic progression of spermatocytes remains to be established. In this study, flow cytometric analyses showed a decrease in haploid, while an increase in tetraploid spermatogenic cells in both 30‐ and 60‐day‐old Ggnbp2 knockout testes. In spread spermatocyte nuclei, Ggnbp2 loss increased DNA double‐strand breaks (DSB), compromised DSB repair and reduced crossovers. Further investigations demonstrated that GGNBP2 co‐immunoprecipitated with a testis‐enriched protein GGN1. Immunofluorescent staining revealed that both GGNBP2 and GGN1 had the same subcellular localizations in spermatocyte, spermatid and spermatozoa. Ggnbp2 loss suppressed Ggn expression and nuclear accumulation. Furthermore, deletion of either Ggnbp2 or Ggn in GC‐2spd cells inhibited their differentiation into haploid cells in vitro. Overexpression of Ggnbp2 in Ggnbp2 null but not in Ggn null GC‐2spd cells partially rescued the defect coinciding with a restoration of Ggn expression. Together, these data suggest that GGNBP2, likely mediated by its interaction with GGN1, plays a role in DSB repair during meiotic progression of spermatocytes.

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Section: Resultsmentioning

confidence: 86%

Ablation of Ggnbp2 impairs meiotic DNA double‐strand break repair during spermatogenesis in mice

Guo

Liu

et al. 2018

J Cellular Molecular Medi

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“…9 Interestingly, the 7-Mb deletion carrier shared uncommon NF1 symptoms with the patient herein described (distinct craniofacial dysmorphisms, congenital heart defect, epileptic seizures, and severe mental retardation). 23 It is noteworthy that the deletion in the reported patient included a cluster of chemokine genes (CCL1, 2, 3,5,7,8,11,12,13,15,16,18, and 23) and four microRNA genes (hsa-mir-423, -193a, -365-2, and -632), deletion of which may contribute to the atypical phenotype. Interestingly, using a new literature-mining bioinformatics approach to prioritize disease genes, based on aGeneApart software, we identified NUFIP2 (nuclear fragile X mental retardation protein interacting protein 2; NM_020772) as a gene whose deregulation might be involved in the reported patient's mental retardation, being statistically associated with mental retardation in MEDLINE abstracts (Po10 À5 ).…”

Section: Discussionmentioning

confidence: 99%

“…12 While little experimental information exists, GGNBP2 could be involved in a process associated with spermatogenesis but might also have a tumor suppressive activity (GGNBP2 is also known as LCRG1 for laryngeal carcinoma-related gene 1). 13,14 As PIPOX and GGNBP2 have the same transcriptional orientation, we suspected the production of a chimeric transcript. We successfully amplified and sequenced this transcript in the propositus, with primers CHIMERIC-U/L designed to hybridize to PIPOX exon 4 and GGNBP2 exon 6, respectively (Figure 3b).…”

Section: Molecular Analysismentioning

confidence: 99%

Characterization of a 7.6-Mb germline deletion encompassing the NF1 locus and about a hundred genes in an NF1 contiguous gene syndrome patient

et al. 2008

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We describe a large germline deletion removing the NF1 locus, identified by heterozygosity mapping based on microsatellite markers, in an 8-year-old French girl with a particularly severe NF1 contiguous gene syndrome. We used gene-dose mapping with sequence-tagged site real-time PCR to locate the deletion end points, which were precisely characterized by means of long-range PCR and nucleotide sequencing. The deletion is located on chromosome arm 17q and is exactly 7 586 986 bp long. It encompasses the entire NF1 locus and about 100 other genes, including numerous chemokine genes, an attractive in silico-selected cerebrally expressed candidate gene (designated NUFIP2, for nuclear fragile X mental retardation protein interacting protein 2; NM_020772) and four microRNA genes. Interestingly, the centromeric breakpoint is located in intron 4 of the PIPOX gene (pipecolic acid oxidase; NM_016518) and the telomeric breakpoint in intron 5 of the GGNBP2 gene (gametogenetin binding protein 2; NM_024835) coding a transcription factor. As PIPOX and GGNBP2 have the same transcriptional orientation, we postulated, and then confirmed, the existence of a chimeric transcript. This transcript, and/or haploinsufficiency of one or several deleted genes, could explain the clinical severity of the syndrome in this patient.

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“…Finally, several proteins identified in our yeast two-hybrid screen are involved in regulating cellular processes other than the actin cytoskeleton. Transmembrane emp24-like trafficking protein 10 (Tmed10) and gametogenetin-binding protein 2 (Ggnbp2) are involved in intracellular protein trafficking (72,83), whereas muscleblind-like RNA-binding proteins, such as muscleblind-like 3 (Mbnl3), inhibit muscle differentiation and regulate alternative splicing of pre-mRNA (25,38,69,74). Overall, the proteins identified in our screen regulate a number of highly ATP-dependent processes, which could require a localized source of ATP provided by CKB in muscle cells.…”

Section: Ckb Is Localized In Both Myocytes and Myotubesmentioning

confidence: 99%

Creatine kinase B is necessary to limit myoblast fusion during myogenesis

Simionescu-Bankston

Pichavant

Canner

et al. 2015

American Journal of Physiology-Cell Physiology

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GK.Creatine kinase B is necessary to limit myoblast fusion during myogenesis. Am J Physiol Cell Physiol 308: C919 -C931, 2015. First published March 25, 2015 doi:10.1152/ajpcell.00029.2015.-Myoblast fusion is critical for proper muscle growth and regeneration. During myoblast fusion, the localization of some molecules is spatially restricted; however, the exact reason for such localization is unknown. Creatine kinase B (CKB), which replenishes local ATP pools, localizes near the ends of cultured primary mouse myotubes. To gain insights into the function of CKB, we performed a yeast two-hybrid screen to identify CKB-interacting proteins. We identified molecules with a broad diversity of roles, including actin polymerization, intracellular protein trafficking, and alternative splicing, as well as sarcomeric components. In-depth studies of ␣-skeletal actin and ␣-cardiac actin, two predominant muscle actin isoforms, demonstrated their biochemical interaction and partial colocalization with CKB near the ends of myotubes in vitro. In contrast to other cell types, specific knockdown of CKB did not grossly affect actin polymerization in myotubes, suggesting other muscle-specific roles for CKB. Interestingly, knockdown of CKB resulted in significantly increased myoblast fusion and myotube size in vitro, whereas knockdown of creatine kinase M had no effect on these myogenic parameters. Our results suggest that localized CKB plays a key role in myotube formation by limiting myoblast fusion during myogenesis.

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Yeast two‐hybrid screens imply that GGNBP1, GGNBP2 and OAZ3 are potential interaction partners of testicular germ cell‐specific protein GGN1

Cited by 48 publications

References 29 publications

Ablation of Ggnbp2 impairs meiotic DNA double‐strand break repair during spermatogenesis in mice

Ablation of Ggnbp2 impairs meiotic DNA double‐strand break repair during spermatogenesis in mice

Characterization of a 7.6-Mb germline deletion encompassing the NF1 locus and about a hundred genes in an NF1 contiguous gene syndrome patient

Creatine kinase B is necessary to limit myoblast fusion during myogenesis

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