Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis最新文献

{"title":"Therapeutic potential of curcumin in autophagy modulation: Insights into the role of transcription factor EB","authors":"Shabnam Radbakhsh ,&nbsp;Prashant Kesharwani ,&nbsp;Amirhossein Sahebkar","doi":"10.1016/j.mrfmmm.2024.111879","DOIUrl":"10.1016/j.mrfmmm.2024.111879","url":null,"abstract":"<div><p>Transcription factor EB (TFEB) is a basic Helix–Loop–Helix/Leucine Zipper (bHLHZip) class of DNA-binding proteins, which can control the expression of genes included in the autophagy–lysosomal pathway. TFEB regulates the autophagic flux by enhancing lysosome biogenesis, forming autophagosomes, and fusion with lysosomes, thereby facilitating cellular clearance of pathogenic protein structures. Curcumin is a natural polyphenolic molecule with pharmacological properties that make it a potential therapeutic candidate for a wide range of diseases. One of the important curcumin mechanisms of action includes modulation of autophagy through affecting various signaling components such as TFEB. This review discusses <em>in vitro</em> and <em>in vivo</em> evidence on the effects of curcumin on autophagy process <em>via</em> modulating TFEB activity in different disorders.</p></div>","PeriodicalId":49790,"journal":{"name":"Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis","volume":"829 ","pages":"Article 111879"},"PeriodicalIF":1.5,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142040854","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transcription factor NFYA inhibits ferroptosis in lung adenocarcinoma cells by regulating PEBP1","authors":"Feng Chen,&nbsp;Tingting Xu,&nbsp;Ni Jin,&nbsp;Digeng Li,&nbsp;Yanfu Ying,&nbsp;Chen Wang","doi":"10.1016/j.mrfmmm.2024.111873","DOIUrl":"10.1016/j.mrfmmm.2024.111873","url":null,"abstract":"<div><h3>Background</h3><p>Ferroptosis is an iron-dependent programmed cell death mediated by lipid peroxidation. The purpose was to explore the molecular mechanism by which phosphatidylethanolamine-binding protein 1 (PEBP1) regulates ferroptosis in lung adenocarcinoma (LUAD), hoping to identify novel therapeutic targets for LUAD.</p></div><div><h3>Methods</h3><p>The expression, enrichment pathways and upstream transcription factors of PEBP1 were analyzed using bioinformatics tools. Dual-luciferase reporter assay and chromatin immunoprecipitation (ChIP) experiments were conducted to validate the interaction and binding relationship between PEBP1 and the upstream transcription factor nuclear transcription factor Y subunit α (NFYA). Quantitative reverse transcription PCR (qRT-PCR) was conducted to measure the expression levels of PEBP1 and NFYA mRNA in LUAD cells. Cell viability was detected by cell counting kit-8 assay. In addition, levels of malondialdehyde (MDA), Fe²⁺, and lipid reactive oxygen species (ROS) were assessed to evaluate ferroptosis levels in LUAD cells.</p></div><div><h3>Results</h3><p>PEBP1 was downregulated and significantly enriched in the ferroptosis signaling pathway in LUAD. Overexpression of PEBP1 suppressed cell viability remarkably, while levels of MDA, Fe²⁺, and lipid ROS were increased. Conversely, knockdown of PEBP1 produced the opposite effects. The upstream transcription factor NFYA, predicted to be involved in the regulation of PEBP1, was also upregulated in LUAD. Dual-luciferase reporter assay, ChIP, and molecular experiments revealed that NFYA transcriptionally suppressed the expression of PEBP1, and overexpression of NFYA could reverse the effects caused by PEBP1 overexpression.</p></div><div><h3>Conclusion</h3><p>PEBP1 regulated ferroptosis in LUAD, and the transcription factor NFYA inhibited ferroptosis in LUAD cells by transcriptionally downregulating PEBP1 expression.</p></div>","PeriodicalId":49790,"journal":{"name":"Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis","volume":"829 ","pages":"Article 111873"},"PeriodicalIF":1.5,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141602398","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Knockdown of SDCBP induces autophagy to promote cardiomyocyte growth and angiogenesis in hypoxia/reoxygenation model","authors":"Ling Gao,&nbsp;Wanqian Liu","doi":"10.1016/j.mrfmmm.2024.111885","DOIUrl":"10.1016/j.mrfmmm.2024.111885","url":null,"abstract":"<div><h3>Objective</h3><div>Angina, myocardial infarction, and even mortality can result from myocardial ischemia (MI). Angiogenesis facilitates tissue repair, lessens cell damage, and ensures that ischemic tissues receive blood and oxygen. This study investigated the possible mechanism of syndecan-binding protein (SDCBP) on autophagy and assessed its impact on myocardial ischemia.</div></div><div><h3>Method</h3><div>A cardiac hypoxia-reoxygenation (H/R) cell model was created for this investigation. Flow cytometry, the cell counting kit-8, and Western blotting were used to measure the damage to cardiomyocytes. Western blotting and immunofluorescence were used to quantify autophagy. Furthermore, assays for tube formation, migration, and Western blotting were used to assess angiogenic capacity. Additionally, the EGFR-PI3K-Akt signaling pathway's activation was found using Western blotting.</div></div><div><h3>Result</h3><div>In the H/R-induced cardiomyocyte model, there is a rise in the expression of SDCBP. Treatment with H/R markedly boosted apoptosis and considerably decreased cell survival. H/R induction strongly inhibits autophagy, increases P62 expression, and decreases LC3II/I expression. Moreover, H/R induction dramatically reduced the ability to form tubes, migrate, and express VEGF, all of which prevented cell angiogenesis. Furthermore, EGFR-PI3K-Akt signaling pathway expression is strongly inhibited by H/R induction. considerable reduction of H/R-induced cell damage, considerable inhibition of apoptosis, promotion autophagy and angiogenesis, and activation of the EGFR-PI3K-Akt signaling pathway are all possible with SDCBP knockdown.</div></div><div><h3>Conclusion</h3><div>To summarize, this study demonstrates that via stimulating the EGFR-PI3K-Akt signaling pathway, SDCBP knockdown may mitigate the effects of H/R-induced cardiomyocyte death and encourage autophagy and blood vessel formation. A theoretical foundation for possible myocardial infarction treatment is thus provided.</div></div>","PeriodicalId":49790,"journal":{"name":"Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis","volume":"829 ","pages":"Article 111885"},"PeriodicalIF":1.5,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142561078","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MicroRNA-532 as a probable diagnostic and therapeutic marker in cancer patients","authors":"Malihe Lotfi ,&nbsp;Amirhosein Maharati ,&nbsp;Amir Abbas Hamidi ,&nbsp;Negin Taghehchian ,&nbsp;Meysam Moghbeli","doi":"10.1016/j.mrfmmm.2024.111874","DOIUrl":"10.1016/j.mrfmmm.2024.111874","url":null,"abstract":"<div><p>The high mortality rate in cancer patients is always one of the main challenges of the health systems globally. Several factors are involved in the high rate of cancer related mortality, including late diagnosis and drug resistance. Cancer is mainly diagnosed in the advanced stages of tumor progression that causes the failure of therapeutic strategies and increases the death rate in these patients. Therefore, assessment of the molecular mechanisms associated with the occurrence of cancer can be effective to introduce early tumor diagnostic markers. MicroRNAs (miRNAs) as the stable non-coding RNAs in the biological body fluids are involved in regulation of cell proliferation, migration, and apoptosis. MiR-532 deregulation has been reported in different tumor types. Therefore, in the present review we discussed the role of miR-532 during tumor growth. It has been shown that miR-532 has mainly a tumor suppressor role through the regulation of transcription factors, chemokines, and signaling pathways such as NF-kB, MAPK, PI3K/AKT, and WNT. In addition to the independent role of miR-532 in regulation of cellular processes, it also functions as a mediator of lncRNAs and circRNAs. Therefore, miR-532 can be considered as a non-invasive diagnostic/prognostic marker as well as a therapeutic target in cancer patients.</p></div>","PeriodicalId":49790,"journal":{"name":"Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis","volume":"829 ","pages":"Article 111874"},"PeriodicalIF":1.5,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141581906","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Apiole, an important constituent of parsley, is a mixed-type inhibitor of the CYP1A subfamily","authors":"J.J. Espinosa-Aguirre ,&nbsp;R. Camacho-Carranza ,&nbsp;SL Hernández-Ojeda ,&nbsp;R.I. Cárdenas-Ávila ,&nbsp;R. Santes-Palacios","doi":"10.1016/j.mrfmmm.2024.111881","DOIUrl":"10.1016/j.mrfmmm.2024.111881","url":null,"abstract":"<div><p>Apiole (1-allyl-2,5-dimethoxy-3,4-methylenedioxybenzene) and parsley leaves ethanolic extract containing it inhibit the rat liver microsomal ethoxy- and methoxyresorufin-<em>O</em>-deacetylase activities associated with cytochrome P450 (CYP) 1A1 and 1A2, respectively. Cytochrome P4501A subfamily metabolizes environmental mutagens and several drugs, leading to the formation of mutagenic metabolites. Docking analysis showed that residue Phe123 within the active site of the CYP1A1 enzyme is bound to apiole through a π/π stacking of its benzene ring. In the case of 1A2, its Phe226 interacts with the dioxolane ring of apiole. Furthermore, apiole behaves as a mixed-type inhibitor of bacterial human recombinant CYP1A1. To explore one of the possible biological implications of this inhibitory effect, we tested the capacity of apiole and the parsley ethanolic extract to interfere with the mutagenicity of the promutagen 2-amino-3,8-dimethylimidazo[4,5-<em>f</em>]quinoxaline (MeIQx) metabolized by CYP1A subfamily. As expected, both apiole and the plant extract reduced the number of revertant colonies of <em>Salmonella typhimurium</em> TA98 Ames strain after exposure to MeIQx, reaching a 78 % and 100 % reduction, respectively. Neither apiol nor parsley extract were mutagenic to the TA98 strain. We speculate that consuming apiole, a constituent of edible herbs, in conjunction with the utilization of pharmaceuticals metabolized by the CYP1A subfamily, may result in herb-drug interactions. Furthermore, the consumption of apiole by individuals who regularly ingest fresh vegetables may contribute to the low incidence of cancer observed in those who adhere to such a dietary regimen.</p></div>","PeriodicalId":49790,"journal":{"name":"Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis","volume":"829 ","pages":"Article 111881"},"PeriodicalIF":1.5,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0027510724000319/pdfft?md5=17daae5a5788ebda9ab86f4f88a2a81b&pid=1-s2.0-S0027510724000319-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142075956","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"KDM4B mutations in human cancers","authors":"Wesley Bush ,&nbsp;Korey Bosart ,&nbsp;Renee A. Bouley ,&nbsp;Ruben C. Petreaca","doi":"10.1016/j.mrfmmm.2024.111866","DOIUrl":"https://doi.org/10.1016/j.mrfmmm.2024.111866","url":null,"abstract":"<div><p>Homologous recombination (HR) is essential for repair of DNA double-strand breaks (DSBs) and restart of stalled or collapsed replication forks. Most cancers are characterized by mutations in components of the DSB repair pathways. Redundant DSB repair pathways exist in eukaryotes from yeast to humans and recent evidence has shown that complete loss of HR function appears to be lethal. Recent evidence has also shown that cancer cells with mutations in one DSB repair pathway can be killed by inhibiting one or more parallel pathways, a strategy that is currently aggressively explored as a cancer therapy. KDM4B is a histone demethylase with pleiotropic functions, which participates in preparing DSBs for repair by contributing to chromatin remodeling. In this report we carried out a pan-cancer analysis of KDM4B mutations with the goal of understanding their distribution and interaction with other DSB genes. We find that although KDM4B mutations co-occur with DSB repair genes, most KDM4B mutations are not drivers or pathogenic. A sequence conservation analysis from yeast to humans shows that highly conserved residues are resistant to mutation. Finally, all mutations occur in a heterozygous state. A single mutation, R986L, was predicted to significantly affect protein structure using computational modeling. This analysis suggests that KDM4B makes contributions to DSB repair but is not a key player.</p></div>","PeriodicalId":49790,"journal":{"name":"Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis","volume":"829 ","pages":"Article 111866"},"PeriodicalIF":2.3,"publicationDate":"2024-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0027510724000162/pdfft?md5=1cd28343fdc40e7e57774491108dc048&pid=1-s2.0-S0027510724000162-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141325622","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HSPE1 enhances aerobic glycolysis to promote progression of lung adenocarcinoma","authors":"Tao Xie ,&nbsp;Manxiang Li","doi":"10.1016/j.mrfmmm.2024.111867","DOIUrl":"https://doi.org/10.1016/j.mrfmmm.2024.111867","url":null,"abstract":"<div><h3>Objective</h3><p>This study aimed to explore the role of heat shock protein family E member 1 (HSPE1) in the metabolism of lung adenocarcinoma (LUAD) cells.</p></div><div><h3>Methods</h3><p>Bioinformatics analysis was applied to examine the expression of HSPE1 in LUAD and its correlation with patient survival. Single-gene Gene Set Enrichment Analysis was conducted for HSPE1. LUAD cell lines or mouse models with up-regulated/down-regulated HSPE1 were constructed. The expression level of HSPE1 was detected by qRT-PCR or immunohistochemical staining. We used CCK-8 assay to measure cell viability and flow cytometry to detect apoptosis levels. Transwell assay was performed to evaluate migration and invasion characteristics. Extracellular Flux Analyzer was employed to detect oxygen consumption rate and extracellular acidification rate. Glucose consumption, adenosine triphosphate production, and lactate levels were measured by Reagent kits. Western blot analysis was conducted to examine the expression levels of GLUT1, HK2, and LDHA.</p></div><div><h3>Results</h3><p>HSPE1 promoted proliferative, migratory, and invasive abilities, and inhibited apoptosis of LUAD cells through the aerobic glycolysis pathway. Specifically, LUAD cells with HSPE1 knockdown exhibited significantly decreased proliferation, migration, and invasion abilities, along with an increased apoptosis rate. Additionally, the expression levels of aerobic glycolysis-related proteins HK2, LADH, and GLUT1 were downregulated, while their levels were increased in LUAD cells with high HSPE1 expression. Suppression of aerobic glycolysis by 2-DG attenuated the promoting effects of HSPE1 overexpression on the proliferation, migration, and invasion of LUAD cells. HSPE1 knockdown inhibited tumor growth and decreased expression levels of HK2, LADH, and GLUT1 <em>in vivo</em>.</p></div><div><h3>Conclusion</h3><p>HSPE1 regulated the proliferation, migration, and invasion of LUAD cells through the aerobic glycolysis pathway, thus facilitating malignant development of LUAD. The study suggested that HSPE1 could be useful as a therapeutic target for LUAD.</p></div>","PeriodicalId":49790,"journal":{"name":"Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis","volume":"829 ","pages":"Article 111867"},"PeriodicalIF":2.3,"publicationDate":"2024-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141325626","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PAX8-AS1/microRNA-25–3p/LATS2 regulates malignant progression of ovarian cancer via Hippo signaling","authors":"Gang Liu,&nbsp;Jing Tian","doi":"10.1016/j.mrfmmm.2024.111858","DOIUrl":"10.1016/j.mrfmmm.2024.111858","url":null,"abstract":"<div><h3>Background</h3><p>Ovarian cancer (OC) is a frequent malignancy of the female reproductive system. Recently, the aberrant expression of numerous lncRNAs has been confirmed as a key factor for cancer development. The regulatory role of PAX8-AS1 in some cancers has been investigated, but its role in OC progression remains unclear. This study focuses on the role and molecular mechanism of PAX8-AS1 in the malignant progression of OC.</p></div><div><h3>Methods</h3><p>Bioinformatics means were adopted to analyze the expression of PAX8-AS1, microRNA-25–3p, and LATS2 in OC tissues and the binding sites between the three. qRT-PCR was employed to determine the expression of these genes in OC cells. CCK-8, colony formation, scratch healing, and Transwell assays were used to see cell viability, proliferation, migration, and invasion, respectively. Fluorescence in situ Hybridization was performed to probe the subcellular localization of PAX8-AS1. Western blot was applied to evaluate the expression and phosphorylation levels of YAP and TAZ, and an immunofluorescence assay was used to detect the translocation of them. Dual luciferase assay was applied to validate the binding relationship between PAX8-AS1 and microRNA-25–3p, as well as between microRNA-25–3p and LATS2.</p></div><div><h3>Results</h3><p>PAX8-AS1 and LATS2 were lowly expressed. MicroRNA-25–3p was highly expressed in OC. PAX8-AS1 was expressed in cytoplasm and regulated LATS2 expression by sponging microRNA-25–3p. Overexpressing PAX8-AS1 can suppress the malignant behaviors of OC cells, whereas treatment with microRNA-mimic can reverse these results. In addition, the phosphorylation levels of YAP and TAZ increased upon oe-LATS2 treatment, and oe-LATS2 could promote YAP and TAZ translocate from the nucleus to cytoplasm. Rescue experiments demonstrated that sh-PAX8-AS1 fostered malignant progression of OC, which was reversed by simultaneous oe-LATS2.</p></div><div><h3>Conclusion</h3><p>In summary, PAX8-AS1/microRNA-25–3p/LATS2 regulated the malignant progression of OC through Hippo signaling, which suggested that PAX8-AS1/microRNA-25–3p/LATS2 axis may be a novel target for OC treatment.</p></div>","PeriodicalId":49790,"journal":{"name":"Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis","volume":"829 ","pages":"Article 111858"},"PeriodicalIF":2.3,"publicationDate":"2024-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141094707","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A pilot study exploring time- and dose-dependent DNA damage and chromosomal instability caused by benzo[a]pyrene in two urothelial cell types","authors":"Jonas Wohlfahrt,&nbsp;Nisha Verma,&nbsp;Rasha Alsaleh,&nbsp;Christian Kersch,&nbsp;Simone Schmitz-Spanke","doi":"10.1016/j.mrfmmm.2024.111855","DOIUrl":"https://doi.org/10.1016/j.mrfmmm.2024.111855","url":null,"abstract":"<div><p>Environmental and occupational exposure to polycyclic aromatic hydrocarbons (PAHs) is associated with adverse health effects in humans. Uncertainty exists regarding the causation of urinary bladder cancer by benzo[<em>a</em>]pyrene (B[<em>a</em>]P) due to a lack of sufficient data. In this work, we focused on <em>in-vitro</em> DNA damage and the formation of micronuclei and chromosomal aberrations as predictors of cancer risk, applying a wide range of dosages and time periods to quantify the onset, intensity, and duration of the response. We chose two urothelial cell types to compare susceptibility and the ability to increase the malignity of a pre-existing bladder cancer: a cancer cell line (T24) and a pooled sample of primary urinary bladder epithelia cells (PUBEC) from pigs. The highest level of DNA damage assessed by comet assay was observed following 24-h treatment in both cell types, whereas PUBEC cells were clearly more susceptible. Even 4-h treatment induced DNA damage in PUBEC cells with benchmark doses of 0.0027 µM B[<em>a</em>]P and 0.00023 µM after 4-h and 24-h exposure, respectively. Nearly no effect was observed for periods of 48 h. The frequency of micronucleus formation increased more markedly in T24 cells, particularly with 24-h treatment. In PUBEC cells, 48-h exposure notably induced the formation of nucleoplasmic bridges and nuclear buds. Even though only one biological replicate was studied due to the sophisticated study design, our results give a strong indication of the potential of B[<em>a</em>]P to induce and increase malignity in human-relevant cell types.</p></div>","PeriodicalId":49790,"journal":{"name":"Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis","volume":"828 ","pages":"Article 111855"},"PeriodicalIF":2.3,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0027510724000058/pdfft?md5=7c8149ac68a4bfa678c29de498ac213f&pid=1-s2.0-S0027510724000058-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140341966","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inducing mutation and ascertaining lethal dosage of in vitro cultures of banana cv. Ney Poovan to ethyl methane sulfonate","authors":"C.Y. Shalini Udaya","doi":"10.1016/j.mrfmmm.2023.111850","DOIUrl":"10.1016/j.mrfmmm.2023.111850","url":null,"abstract":"<div><p><span><span>In vitro mutation breeding in vegetatively propagated crops like banana offers a benefit in screening for beneficial variants in plant cells or cultured tissues. An attempt was made to induce mutants and determine the lethal dose, as it is the prerequisite to optimize the concentration and duration of the mutagen used to recover a larger population in mutation research. </span>Shoot tip cultures<span> were treated for 2 and 4 h at six different EMS<span> concentrations ranging from 80 mM to 160 mM, whereas proliferating multiple shoots were exposed for 30 and 60 min at six different EMS concentrations ranging from 8 mM to 40 mM. Survival percentage, shoot length, and number of shoots reduced linearly and significantly as concentration and duration increased in both shoot tips and proliferating multiple buds. The probit curve-based analysis of mortality of treated explants revealed that the LD</span></span></span>₅₀ was 155.83 mM for 2 h and 113.72 mM for 4 h, respectively for shoot tip cultures, whereas for proliferating multiple buds, the LD₅₀ value was adjusted to 39.11 mM for 30 min and 30.41 mM for 60 min. 160 mM EMS for 4 h resulted in a shorter shoot, a longer rooting duration, a lesser number of roots, and decreased root development. In proliferating multiple shoots, the smallest shoot, longest rooting duration, least number of roots, and shortest root were observed in 40 mM EMS for 60 min. Similar reductions in growth parameters were observed in proliferating multiple shoots at higher exposure to EMS for a longer duration.</p></div>","PeriodicalId":49790,"journal":{"name":"Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis","volume":"828 ","pages":"Article 111850"},"PeriodicalIF":2.3,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138818994","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}