Abstract
Cell division and chromosome replication are tightly coordinated in bacteria. The dipM gene in Caulobacter crescentus is known to be involved in cell division, but its role in chromosome replication remains unclear; previously, a dipM mutant was found to be capable of replication but not of maintaining a plasmid. This study investigates dipM’s function in both processes and aims to identify interacting genes. We hypothesize that dipM regulates chromosome replication through interactions with cell cycle proteins. To test this, a mutagenesis test will be conducted to isolate Caulobacter mutants with replication defects, and we expect to identify mutations that disrupt chromosome replication. Fluorescence-labeled replication reporters will be used to detect cell cycle abnormalities, likely revealing mislocalized replication proteins in dipM mutants. Genetic complementation will be used to determine whether introducing wild-type dipM can restore normal replication and division. We will use a whole-genome library alongside DNA sequencing to identify affected genes, predicting new regulatory components within this pathway. Finally, bioinformatics tools such as BLAST will be used to analyze these genes, potentially uncovering conserved mechanisms of bacterial cell cycle regulation. This study is expected to provide insight into bacterial cell cycle regulation; however, potential genetic redundancy and the need for further validation may pose challenges. Ultimately, this study has the potential to inform research on microbial genetics and antimicrobial development.
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