scholarly journals The spontaneous chlorophyll mutation frequency in barley

Hereditas ◽  
2008 ◽  
Vol 105 (1) ◽  
pp. 71-72 ◽  
Author(s):  
J. HELMS JØRGENSEN ◽  
H. P. JENSEN
Keyword(s):  
Mutation Frequency ◽  
Chlorophyll Mutation

scholarly journals Induction of chlorophyll mutation through physical and chemical mutagen in Phaseolus lunatus (Lima Bean)

2020 ◽  
Vol 26 (1) ◽  
Author(s):  
Kalyani R Gunjal ◽  
A.D. More
Keyword(s):  
Gamma Rays ◽  
Mutation Frequency ◽  
Lima Bean ◽  
Mutation Breeding ◽  
Phaseolus Lunatus ◽  
Chlorophyll Mutation ◽  
Dose Concentration ◽  
Chlorophyll Mutants ◽  
Physical And Chemical ◽  
Light Green

The present investigation was undertaken to study the frequency of chlorophyll deficient sectors and chlorophyll mutants induced by Gamma rays at the dosage of 240Gy,300Gy,360Gy,420Gy, Ethyl Methene Sulphate (EMS) at the concentrations of 0.25%,0.50%,0.75%,1% and the Combination of both (Gamma rays and EMS) like 240Gy+1%, 300Gy+0.75%, 360Gy+0.50%, 420Gy+0.25% in the variety ‘King of Garden’ Phaseolus lunatus (lima bean).The chlorophyll mutants were observed in all the three mutagenic treatments in the lima bean. These mutants were White (Albina), Yellow (Xantha), Yellow green (Chlorina) and Light green (Viridis). They were screened after 10-15 days of old seedling and were found at the margin of the leaflet or the entire leaflet.Induced mutation in the sectors of the leaves resulted into chlorophyll chimeric plants. The scoring of chlorophyll mutation frequency in M2 generation was one of the most reliable measures for evaluating the mutagenic induced genetic altercation of the mutagen treatments used in the ideotype. The frequency of chlorophyll mutants increased with the increase in the dose/concentration of the mutants. They can be screened and enhanced through mutation breeding for enormous yield.

scholarly journals Study on mutagenic effectiveness and efficiency of mutagens in inducing chlorophyll mutations in m2 generation in sorghum [Sorghum bicolor (L.) Moench ]

2020 ◽  
Vol 15 (2) ◽  
pp. 107-112
Author(s):  
S.M. Surashe ◽  
H.V. Kalpande ◽  
S.B. Borgaonkar
Keyword(s):  
Gamma Irradiation ◽  
Sorghum Bicolor ◽  
Mutation Frequency ◽  
Chlorophyll Mutation ◽  
Chlorophyll Mutations ◽  
Chlorophyll Mutants ◽  
Mutagenic Sensitivity ◽  
Effectiveness And Efficiency ◽  
Dose Dependent ◽  
Sorghum Bicolor L

An investigation was carried out to create the variability generated through induced mutation in two sorghum populations viz., 296 B (Kharif) and Parbhani Moti (Rabi). Two mutagens viz., gamma irradiation (10 kR, 20kR, 30kR and 40kR) and EMS (0.1%EMS, 0.2%EMS, 0.3%EMS and 0.3%EMS) and their combination were used M2 generation. Mutagenic sensitivity in M2 generation on the basis of reduced germination and plant survival revealed a dose dependent reaction and differential response of the populations. In general, chlorophyll mutation frequency expressed on M2 seedling basis increased linearly with doses of three the mutagens in 296 B and Parbhani Moti. The frequency was more in 296 B followed by Parbhani Moti of three mutagens. The spectrum of chlorophyll mutations comprised albina, xantha, viridis, xanthaviridis, chlorina. The most frequently occurred mutant was viridis type followed by chlorina in all the populations. The population 296 B had expressed largest frequency of chlorophyll mutants followed by Parbhani Moti.

Change in mutation frequency at a TP53 hotspot during culture of ENU-mutagenised human lymphoblastoid cells

Mutagenesis ◽  
2019 ◽  
Author(s):  
Masahiko Watanabe ◽  
Masae Toudou ◽  
Taeko Uchida ◽  
Misato Yoshikawa ◽  
Hiroaki Aso ◽  
...  
Keyword(s):  
Cell Culture ◽  
Cell Growth ◽  
Mutation Frequency ◽  
Cultured Cells ◽  
Tp53 Gene ◽  
Tumour Suppressor Genes ◽  
Restriction Sites ◽  
Mutation Spectra ◽  
Risk Of Cancer ◽  
Assay Conditions

Abstract Mutations in oncogenes or tumour suppressor genes cause increases in cell growth capacity. In some cases, fully malignant cancer cells develop after additional mutations occur in initially mutated cells. In such instances, the risk of cancer would increase in response to growth of these initially mutated cells. To ascertain whether such a situation might occur in cultured cells, three independent cultures of human lymphoblastoid GM00130 cells were treated with N-ethyl-N-nitrosourea to induce mutations, and the cells were maintained for 12 weeks. Mutant frequencies and spectra of the cells at the MspI and HaeIII restriction sites located at codons 247–250 of the TP53 gene were examined. Mutant frequencies at both sites in the gene exhibited a declining trend during cell culture and reached background levels after 12 weeks; this was also supported by mutation spectra findings. These results indicate that the mutations detected under our assay conditions are disadvantageous to cell growth.

scholarly journals Revealing the Roles of Keratin 8/18-Associated Signaling Proteins Involved in the Development of Hepatocellular Carcinoma

2021 ◽  
Vol 22 (12) ◽  
pp. 6401
Author(s):  
Younglan Lim ◽  
Nam-On Ku
Keyword(s):  
Hepatocellular Carcinoma ◽  
Transcription Factors ◽  
Liver Damage ◽  
Cell Shape ◽  
Mutation Frequency ◽  
Cytoskeletal Proteins ◽  
Signaling Proteins ◽  
Intermediate Filament Proteins ◽  
Keratin 8 ◽  
Keratin 18

Although hepatocellular carcinoma (HCC) is developed with various etiologies, protection of hepatocytes seems basically essential to prevent the incidence of HCC. Keratin 8 and keratin 18 (K8/K18) are cytoskeletal intermediate filament proteins that are expressed in hepatocytes. They maintain the cell shape and protect cells under stress conditions. Their protective roles in liver damage have been described in studies of mouse models, and K8/K18 mutation frequency in liver patients. Interestingly, K8/K18 bind to signaling proteins such as transcription factors and protein kinases involved in HCC development. Since K8/K18 are abundant cytoskeletal proteins, K8/K18 binding with the signaling factors can alter the availability of the factors. Herein, we discuss the potential roles of K8/K18 in HCC development.

scholarly journals Nucleoside Analogues Are Potent Inducers of Pol V-mediated Mutagenesis

Biomolecules ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 843
Author(s):  
Balagra Kasim Sumabe ◽  
Synnøve Brandt Ræder ◽  
Lisa Marie Røst ◽  
Animesh Sharma ◽  
Eric S. Donkor ◽  
...  
Keyword(s):  
Mammalian Cells ◽  
Mutation Frequency ◽  
Nucleoside Analogues ◽  
Cancer Therapies ◽  
E Coli ◽  
Replicative Stress ◽  
Pol V ◽  
Dna And Rna ◽  
Sos Induction ◽  
Anti Cancer

Drugs targeting DNA and RNA in mammalian cells or viruses can also affect bacteria present in the host and thereby induce the bacterial SOS system. This has the potential to increase mutagenesis and the development of antimicrobial resistance (AMR). Here, we have examined nucleoside analogues (NAs) commonly used in anti-viral and anti-cancer therapies for potential effects on mutagenesis in Escherichia coli, using the rifampicin mutagenicity assay. To further explore the mode of action of the NAs, we applied E. coli deletion mutants, a peptide inhibiting Pol V (APIM-peptide) and metabolome and proteome analyses. Five out of the thirteen NAs examined, including three nucleoside reverse transcriptase inhibitors (NRTIs) and two anti-cancer drugs, increased the mutation frequency in E. coli by more than 25-fold at doses that were within reported plasma concentration range (Pl.CR), but that did not affect bacterial growth. We show that the SOS response is induced and that the increase in mutation frequency is mediated by the TLS polymerase Pol V. Quantitative mass spectrometry-based metabolite profiling did not reveal large changes in nucleoside phosphate or other central carbon metabolite pools, which suggests that the SOS induction is an effect of increased replicative stress. Our results suggest that NAs/NRTIs can contribute to the development of AMR and that drugs inhibiting Pol V can reverse this mutagenesis.

scholarly journals THE INTERCELLULAR DISTRIBUTION OF MUTATIONS INDUCED IN OOCYTES OF DROSOPHILA MELANOGASTER BY CHEMICAL AND PHYSICAL MUTAGENS

Genetics ◽  
1979 ◽  
Vol 92 (1) ◽  
pp. 151-160
Author(s):  
H Traut
Keyword(s):  
Drosophila Melanogaster ◽  
Mitomycin C ◽  
Mutation Frequency ◽  
Lethal Mutation ◽  
X Rays ◽  
Mutagenic Treatment ◽  
X Chromosomes ◽  
Recessive Lethal ◽  
Lethal Mutations ◽  
X Irradiation

ABSTRACT When females of Drosophila melanogaster are treated with chemical or physical mutagens, not only in one but also in both of the two homologous X chromosomes of a given oocyte, a recessive sex-linked lethal mutation may be induced. A method is described that discriminates between such "single" and "double mutations." A theory is developed to show how a comparison between the expected and the observed frequency of double mutations yields an indication of the intercellular distribution (random or nonrandom) of recessive lethal mutations induced by mutagenic agents in oocytes and, consequently, of the distribution (homogeneous or nonhomogeneous) of those agents.—Three agents were tested: FUdR (12.5, 50.0 and 81.0,μg/ml), mitomycin C (130.0 μg/ml) and X rays (2000 R, 150 kV). After FUdR feeding, no increase in the mutation frequency usually observed in D. melanogaster without mutagenic treatment was obtained (u=0.13%, namely three single mutations among 2332 chromosomes tested). After mitomycin C feeding, 104. single and three double mutations were obtained. All of the 50 mutations observed after X irradiation were single mutations. The results obtained in the mitomycin C and radiation experiments favor the assumption of a random intercellular distribution of recessive lethal mutations induced by these two agents in oocytes of D. melanogaster. Reasons are discussed why for other types of mutagenic agents nonrandom distributions may be observed with our technique.

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