TBCEL antibody - C - terminal region (OAAB08694)
- Known as:
- TBCEL (anti-) - C - terminal region (OAAB08694)
- Catalog number:
- oaab08694
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- TBCEL antibody - terminal region (OAAB08694)
Related genes to: TBCEL antibody - C - terminal region (OAAB08694)
- Gene:
- TBCEL NIH gene
- Name:
- tubulin folding cofactor E like
- Previous symbol:
- LRRC35
- Synonyms:
- MGC10233
- Chromosome:
- 11q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2005-03-13
- Date modifiied:
- 2016-06-17
Related products to: TBCEL antibody - C - terminal region (OAAB08694)
Related articles to: TBCEL antibody - C - terminal region (OAAB08694)
- The interspecific hybrid scallops generated from the hermaphroditic bay scallops (Argopecten irradians) and Peruvian scallops (Argopecten purpuratus) showed significant heterosis in growth. However, its sterility limits large-scale hybridization and hinders the development of the scallop breeding industry. Hybrid sterility is regulated by plenty of genes and involves a range of biochemical and physiological transformations. In this study, whole-genome re-sequencing and transcriptomic analysis were performed in sterile and fertile hybrid scallops. The potential genetic variations and abnormally expressed genes were detected to explore the mechanism underlying hybrid sterility in hermaphroditic Argopecten scallops. Compared with fertile hybrids, 24 differentially expressed genes (DEGs) with 246 variations were identified to be related to fertility regulation, which were mainly enriched in germarium-derived egg chamber formation, spermatogenesis, spermatid development, mismatch repair, mitotic and meiotic cell cycles, Wnt signaling pathway, MAPK signaling pathway, calcium modulating pathway, and notch signaling pathway. Specifically, variation and abnormal expression of these genes might inhibit the progress of mitosis and meiosis, promote cell apoptosis, and impede the genesis and maturation of gametes in sterile hybrid scallops. Eleven DEGs (XIAP, KAZN, CDC42, MEIS1, SETD1B, NOTCH2, TRPV5, M- EXO1, GGT1, SBDS, and TBCEL) were confirmed by qRT-PCR validation. Our findings may enrich the determination mechanism of hybrid sterility and provide new insights into the use of interspecific hybrids for extensive breeding. - Source: PubMed
Publication date: 2023/08/26
Yu TieyingNing JunhaoWang FukaiLiu GuilongWang QuanchaoXu XinWang ChundeLu Xia - Individual sperm cells are resolved from a syncytium during late step of spermiogenesis known as individualization, which is accomplished by an Individualization Complex (IC) composed of 64 investment cones. encodes Tubulin-binding cofactor E-like (TBCEL), suggesting a role for microtubule dynamics in individualization. Indeed, a population of ∼100 cytoplasmic microtubules fails to disappear in mutant testes during spermatogenesis. This persistence, detected using epi-fluorescence and electron microscopy, suggests that removal of these microtubules by TBCEL is a prerequisite for individualization. Immunofluorescence reveals TBCEL expression in elongated spermatid cysts. In addition, testes from mutant males were rescued to wild type using to drive TBCEL expression, indicating that the mutant phenotype is caused by the lack of TBCEL. Finally, RNAi driven by -GAL4 successfully phenocopied , confirming that is required in the germline for individualization. We propose a model in which the cytoplasmic microtubules serve as alternate tracks for investment cones in mutant testes.This article has an associated First Person interview with the first author of the paper. - Source: PubMed
Publication date: 2020/02/26
Fabrizio James JRollins JanetBazinet Christopher WWegener StephanieKoziy IrynaDaniel RachelLombardo VincentPryce DwaineBharrat KavitaInnabi ElissaVillanobos MarielleMendoza GabrielaFerrara ElisaRodway StephanieVicioso MatthewSiracusa VictoriaDailey ErinPronovost JustinInnabi SimonPatel VrutantDeSouza NicoleQuaranto DanielleNiknejad Amir - The evolution of metazoans from their choanoflagellate-like unicellular ancestor coincided with the acquisition of novel biological functions to support a multicellular lifestyle, and eventually, the unique cellular and physiological demands of differentiated cell types such as those forming the nervous, muscle and immune systems. In an effort to understand the molecular underpinnings of such metazoan innovations, we carried out a comparative genomics analysis for genes found exclusively in, and widely conserved across, metazoans. Using this approach, we identified a set of 526 core metazoan-specific genes (the 'metazoanome'), approximately 10% of which are largely uncharacterized, 16% of which are associated with known human disease, and 66% of which are conserved in Trichoplax adhaerens, a basal metazoan lacking neurons and other specialized cell types. Global analyses of previously-characterized core metazoan genes suggest a prevalent property, namely that they act as partially redundant modifiers of ancient eukaryotic pathways. Our data also highlights the importance of exaptation of pre-existing genetic tools during metazoan evolution. Expression studies in C. elegans revealed that many metazoan-specific genes, including tubulin folding cofactor E-like (TBCEL/coel-1), are expressed in neurons. We used C. elegans COEL-1 as a representative to experimentally validate the metazoan-specific character of our dataset. We show that coel-1 disruption results in developmental hypersensitivity to the microtubule drug paclitaxel/taxol, and that overexpression of coel-1 has broad effects during embryonic development and perturbs specialized microtubules in the touch receptor neurons (TRNs). In addition, coel-1 influences the migration, neurite outgrowth and mechanosensory function of the TRNs, and functionally interacts with components of the tubulin acetylation/deacetylation pathway. Together, our findings unveil a conserved molecular toolbox fundamental to metazoan biology that contains a number of neuronally expressed and disease-related genes, and reveal a key role for TBCEL/coel-1 in regulating microtubule function during metazoan development and neuronal differentiation. - Source: PubMed
Publication date: 2013/10/03
Frédéric Melissa YLundin Victor FWhiteside Matthew DCueva Juan GTu Domena KKang S Y CatherineSingh HansmeetBaillie David LHutter HaraldGoodman Miriam BBrinkman Fiona S LLeroux Michel R - The tubulin-specific chaperone E-like protein (TBCEL or E-like) of vertebrates shows sequence homology to TBCE, a component of the multimolecular complex required for tubulin heterodimer formation in all eukaryotic cells. TBCEL apparently serves more specific functions, as it is found only in animals. At the cellular level, TBCEL plays a role as a regulator of tubulin stability. It is strongly expressed in human testes, but its systemic function is not known. The gene CG12214 codes for the Drosophila homologue of the vertebrate TBCEL protein. Here we show that disruption of the Drosophila Tbcel gene causes defects in spermatid individualixation, which leads to dispersed migration of F-actin-rich investment cones. Mutations affecting the Tbcel gene cause strong reduction in male, but not female, fertility. However, mature sperm function apparently is not impaired. We generated polyclonal antisera against TBCEL to study its localization and distribution in Drosophila tissues. Immunostainings of wild-type and null mutant testes demonstrated that TBCEL is localized in testes, presumably associated with axoneme bundles prior to spermatid individualization. Molecular analysis of the transposon insertion site in the mutant mulet (mlt), for which male sterility and sperm individualization defects have previously been described, demonstrates that the mlt P-element insertion resides in the Tbcel gene. Our results show that loss of TBCEL in Drosophila is compatible with viability and normal female fertility but causes reduced male fertility. We conclude that Drosophila TBCEL is strongly expressed in testes and plays an important role in sperm individualization during spermatogenesis. The high level of Tbcel mRNA in human testes suggests a general role of TBCEL in animal spermatogenesis. However, Western blots and courtship analysis suggest that TBCEL may have additional functions in the nervous system of Drosophila that could contribute to the observed reduced male fertility. These functions now have to be investigated. - Source: PubMed
Publication date: 2012/11/02
Nuwal TulipKropp MarleneWegener StephanieRacic SonjaMontalban ItsasoBuchner Erich - Notch proteins are definitely recognized as key regulators of the neuronal fate during embryo development, but their function in the adult brain is still largely unknown. We have previously demonstrated that Notch pathway stimulation increases microtubules stability followed by the remodeling of neuronal morphology with neurite varicosities loss, thicker neuritis, and enlarged growth cones. Here we show that the neurite remodeling is a dynamic event, dependent on transcription and translation, and with functional implications. Exposure of differentiated human SH-SY5Y neuroblastoma cells to the Notch ligand Jagged1 induces varicosities loss all along the neurites, accompanied by the redistribution of presynaptic vesicles and the decrease in neurotransmitters release. As evaluated by time lapse digital imaging, dynamic changes in neurite morphology were rapidly reversible and dependent on the activation of the Notch signaling pathway. In fact, it was prevented by the inhibition of the proteolytic gamma-secretase enzyme or the transcription machinery, and was mimicked by the transfection of the intracellular domain of Notch. One hour after treatment with Jagged1, several genes were downregulated. Many of these genes encode proteins that are known to be involved in protein synthesis. These data suggest that in adult neurons, Notch pathway activates a transcriptional program that regulates the equilibrium between varicosities formation and varicosities loss in the neuronal presynaptic compartment involving the expression and redistribution of both structural and functional proteins. - Source: PubMed
Ferrari-Toninelli GiuliaBonini Sara AnnaUberti DanielaNapolitano FrancescoStante MariaSantoro FedericaMinopoli GiuseppinaZambrano NicolaRusso TommasoMemo Maurizio