Cell division is controlled by nuclear genes
2-min read | Biology
As you may know already, the body is composed of billions of tiny structures called cells. The cell is the basic unit of life. You may wonder how does the body get so many cells? This happens through a process called the cell cycle where cells grow and divide.
The cell cycle involves the transformation and progression of the cell from a state of growth and resting called G₁ to gene replication or the synthesis state called S. Then the cell enters the second growth phase or G₂ before it enters cell division, which is called mitosis (M). The process begins again with interphase of G₁.
The cell cycle is controlled by special instructions found inside the cell called genes. The genes that control these events are found in the nucleus, which is a special structure within most cells. In human cells, which are a type of animal cell, most genes are found in the nucleus.
According to Amy Chow (2010), a scientist who studies the cell cycle, there are two types of genes that control cell division. These are oncogenes and tumor suppressor genes, that each control the cell cycle. Oncogenes, which give rise to cancer-causing genes, mediate cell division, “allowing cells to proceed from one cell cycle stage to the next.” Conversely, tumor suppressor genes, such as p53, stop cell division by binding to damaged DNA, signaling the cell of a problem mutation. Mutations are changes in the genes that happen over time. Some mutations are bad, some are good, and so have no effect on the cell. Mutations in the p53 gene and the p53 protein have been linked to cancer, which is uncontrolled cell growth.
Source: Chow, A. Y. (2010) Cell Cycle Control by Oncogenes and Tumor Suppressors: Driving the Transformation of Normal Cells into Cancerous Cells. Nature Education 3(9):7 [Available Online]
Image: Cho Y, Gorina S, Jeffrey PD, Pavletich NP. (1994) Crystal structure of a p53 tumor suppressor-DNA complex: understanding tumorigenic mutations. Science. 265 (5170): 346-355. doi:10.1126/science.8023157 [Available Online}