Your team has posed the question: Does MAD1 control the metaphase checkpoint? The hypothesis was: If MAD1 gives the signal to progress to anaphase after chromosomes have aligned, then a group of mutant MAD1 cells will more often have imperfect chromosome numbers after a series of cell divisions compared to normal cells.You investigated this question by comparing the cell division of cells that have the normal, or “wildtype” MAD1 gene to the division of cells with the mutant MAD1 gene. In your experiments, you compared the number of “aneuploid” cells (imperfect chromosome numbers) to the number of “euploid” (correct chromosome numbers) in your experimental group of MAD1 mutant cells and your control group of MAD1 normal cells.
Results: Average Percent of Aneuploid Cells after 24 hrs
Control:Normal MAD1 cells had an average of 10 percent aneuploid cells after 24 hours.
Experimental: Mutatnt MAD1 cells had an average of 30 percent aneuploid cells after 24 hours
Question:
What new questions or future directions could be suggested by the data? Provide an example.
Remember that most regulation and movement of cell structures are controlled by proteins. Speculate on other proteins that might affect aspects of cell division and potentially be involved in cancer.
The mitotic checkpoints are important at the time of mitosis cell division, which are used to inhibit formation of anuploid cell and instaility of chromosome. MAD1 is such as example of mitotic assembly check point protein, whose absence will produce aneuploidy. Now, as chromosomal instability and generations of anuploid cells are observed in several types of cancer, it has been found that MAD1 expression is also downregulated in different cancer.
Now, if we look at cancer, in majority of cancer the gene p53 is mutated. p53 gene is tumor suppresor and is take part important role in controlling cell cycle events, repair of DNA damage or apoptosis. p53 can regulate several genes as downstream target. Here, we can question further whether p53 can also control MAD1.
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