Bacterial cells that can save resources and energy have an advantage over those that cannot. As a result, natural selection has rewarded bacteria that express just the genes whose products the cell needs.

Consider a lone Escherichia coli (abbreviated for E. coli) cell living in the unpredictable environment of a human colon, reliant on its host's erratic eating habits for nutrition. If the bacterium's environment lacks the amino acid tryptophan, which it requires to thrive, the cell responds by initiating a metabolic pathway that produces tryptophan from another molecule. If the human host consumes a tryptophan-rich meal later, the bacterial cell stops proliferating.

A metabolic process can be regulated on two levels, as seen in the image attached, Figure 18.2 for tryptophan production.

To begin, cells can modify the activity of enzymes that are already present. This is a rather quick reaction that relies on numerous enzymes' sensitivity to chemical stimuli that enhance or decrease their catalytic activity.

The activity of the first enzyme in the route is suppressed by the pathway's end product, in this instance tryptophan (as shown in the image attached, Figure 18.2a). As a result, if tryptophan builds up in a cell, it inhibits the production of additional tryptophan by blocking enzyme activity.

This type of feedback inhibition, which is common in anabolic (biosynthetic) pathways, allows a cell to respond to short-term stress.

Inhibition of Normal Cell Signaling Pathways as many proto-oncogenes and tumor suppressor genes encode proteins that are involved in cell signaling pathways.

Regular cells and the problems with their activity in cancerous cells. We shall concentrate on the products of two important genes, the ras proto-oncogene, and the tumor suppressor gene p53. Ras mutations are seen in around 30% of human malignancies, and p53 mutations account for more than half of all cases.

Cell cycle–stimulating mechanism in both normal and mutant cells. A growth factor attaches to its receptor in the plasma membrane, activating the usual route. The signal is transmitted to Ras, a G protein.

Ras, like all G proteins, becomes active when GTP binds to it. Ras sends the signal to four different protein kinases. The final kinase activates 5 a transcription factor (activator) that switches on one or more genes for 6 a protein that promotes cell cycle progression. (b) Excessive cell division and cancer may occur from a mutation that renders Ras or any other pathway component excessively active.

An intracellular signal triggers the production of a protein that inhibits the cell cycle. In this scenario, the signal is damage to the cell's DNA, maybe as a result of UV radiation exposure.

The activation of this signaling pathway halts the cell cycle until the damage is healed. Otherwise, the damage might cause mutations or chromosomal abnormalities, which could contribute to tumor development. As a result, the genes for the pathway's components function as tumor-suppressor genes.

The p53 gene is a tumor suppressor gene called after the 53,000-dalton molecular weight of its protein product. It encodes a particular transcription factor that stimulates the production of cell cycle–inhibitory proteins.

The Ras protein is a G protein that transfers a signal from a growth factor receptor on the plasma membrane to a cascade of protein kinases (as shown in the image attached below). It is encoded by the ras gene (called after rat sarcoma, a connective tissue cancer).

The biological reaction at the pathway's end is the production of a protein that activates the cell cycle (as shown in the image attached below, Figure 18.24a). Normally, such a route will not function until activated by the right growth factor. However, some mutations in the ras gene can result in the creation of a hyperactive Ras protein, which can activate the kinase cascade even in the absence of a kinase cascad

The p53 gene is known as the "guardian angel of the genome." When the gene is triggered, such as by DNA damage, the p53 protein acts as an activator for numerous other genes.

It frequently activates a gene called p21, the product of which stops the cell cycle by attaching to cyclin-dependent kinases, giving the cell time to repair the DNA. Researchers have discovered that p53 stimulates the production of a set of miRNAs, which inhibits the cell cycle.

Furthermore, the p53 protein has the ability to activate genes directly involved in DNA repair. Finally, when DNA damage is irreversible, p53 activates “suicide” genes, the protein products of which cause programmed cell death (apoptosis).

The numerous activities of p53 point to a complicated picture of control in normal cells that we do not completely comprehend.

A recent study may highlight the protective effect of p53 while shedding light on a long-standing research question: Why is cancer so uncommon in elephants? In zoo-based research, the incidence of cancer among elephants has been estimated to be around 3%, compared to closer to 30% in people.

Elephants contain 20 copies of the p53 gene, compared to one copy in humans, other animals, and even manatees, elephants' closest living relatives, according to genome sequencing. There are certainly other factors at work, but the link between low cancer risk and additional copies of the p5 gene seems compelling.