When the timing or strict control over the cell cycle is altered, the dividing cells may become cancerous, as cancer is in many ways a disease of cell division.

When the timing or strict control over the cell cycle is altered, the dividing cells may become cancerous, as cancer is in many ways a disease of cell division.

You and your colleagues are studying a protein called Mitosis Arrest Deficient 1, or MAD1, that appears to be mutated in several human cancers. You suspect that this protein is involved in controlling the metaphase signal giving “the OK” that all chromosomes have aligned at the equator. You think that when this mutated protein is not functional, then anaphase progresses before all the cell’s chromosomes have aligned. The daughter cells will inherit an imperfect number of chromosomes, a condition called “aneuploidy.” Aneuploidy genetic defects can promote cancer.

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. Every sample began with 100 cells which divided over time. You tested four samples for your experimental group and four samples for your control group. The cells were in the same growth conditions including nutrients, oxygen, temperature, humidity, and light. The experiment lasted for 24 hours. At the end of 24 hours, you counted the number of aneuploid cells in each sample. The results are found below: