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In recent years, the demand of chilli has tremendously increased due to its attractive market price and multifarious used in cooked and processed forms. At present people are much concerned about the fruit quality and yield. Therefore, attention is being paid for development of genotypes having high yield potential with desirable fruit quality characters in a short period of time. For this purpose, seeds of chilli were mutagenised with ethyl methane sulphonate (EMS) and diethyl sulphate (DES) to determine their mutagenic sensitivity in M1 generation. The increasing concentration of EMS and DES decreased in morphological and yield characters. The spectrum of mutation and induced variability for various quantitative traits were observed in M1 generation such as germination (%), plant height, primary and secondary branches per plant, days to first flowering, fruit length (cm), fruit girth (cm), total number of fruits per plant, number of seeds per fruit, seed weight per fruit (g), 100 seed weight (g) and pericarp: seed ratio showed variability in chilli with the effect of EMS and DES. The percentage of chromosomal abnormalities in different mitotic stages was significantly higher than that of the control in all the treatment concentrations.
Cell cycle checkpoints are the surveillance mechanisms monitoring both the fidelity and accuracy of DNA replication and the segregation of chromosomes. By delaying progression through the cell cycle, checkpoints provide more time for repair before the critical phases of DNA replication and ensure the proper segregation of chromosomes during mitosis. The paper provides basic information about the molecular mechanisms operating in various cell cycle checkpoints activated by DNA damage or disturbances in mitotic spindle assembly.
To study phosphorylation of D. melanogaster nuclear lamins in vivo, we used KC tissue culture cells. KC cells contain products of both lamin genes, the lamin Dm0 gene encoding constitutive polypeptides expressed in almost all cell types and the developmentally regulated lamin C gene. We grew KC cells in low phosphate medium and labelled them with [32P]H3PO4. To obtain mitotic cells we used vinblastine to arrest cells in metaphase. Cells were collected, washed, lysed and resultant extracts fractionated in the presence of protein phosphatase inhibitors. D. melanogaster proteins were then denatured by boiling in SDS plus DTT, followed by immunoaffinity chromatography and SDS-PAGE purification. As anticipated, we found that a CNBr fragment derived from the N-terminal part of lamin Dm0-derivatives (amino acid residues 2-158; fragment A) was phosphorylated during both interphase and mitosis. Interphase but not mitotic phosphorylation was found on an internal CNBr fragment (derived from the end of the central rod domain and the first part of the C-terminal lamin tail; amino acid residues 385-548; fragment D). Interphase only phosphorylation was also detected on another CNBr fragment derived from the extreme C-terminal portion of lamin Dm0-derivatives (amino acid residues 549-622; fragment E). To supplement these data, we used 2-D tryptic peptide mapping followed by phosphorImager analysis. We routinely detected at least seven ‘spots’ derived from interphase lamins but only a single mitotic lamin phosphopeptide.
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