Researchers at the Duke Institute for Genome Sciences and Policy have unveiled the hitherto unknown characteristics of an on-off switch that controls cell growth.
The researchers have shown that cells, whether damaged or not, keep on dividing if the switch is on.
According to them, the understanding as to how the switch works may be very useful in spotting novel drug targets for cancer, and other diseases that result from a defected cell growth function.
The researchers describe the switch as part of a critical pathway that controls cell division, the process by which the body makes new cells.
Generally, before starting to divide, a cell goes through a checklist to ensure that everything is okay, and it halts the process if it senses that something is wrong. However, as the cell passes a milestone called the restriction point, there is no turning back.
The researchers say that the switch, which is a part of the Rb-E2F signalling pathway, controls this milestone.
While Rb (retinoblastoma) is a key tumour suppressor gene, E2F is a transcription factor that governs the expression of all the genes important for cells to grow.
"The wiring diagram is fundamentally the same. It's very likely that different organisms have evolved a very conserved design principle to regulate their growth," Nature magazine quoted Dr. Guang Yao, lead study author and a postdoctoral fellow in Duke's department of molecular genetics and microbiology, as saying.
The researchers say that the cellular pathway that carries this switch is found in all multi-cellular lives, ranging from plants to people. A cell triggers that pathway when it receives an external chemical signal to grow, they add.
During the course of study, the research team observed an unexpected property of the switch — once turned on by an external signal, the switch could maintain its on state even when the signal disappeared.
The researchers have also broken down the pathway into individual chemical reactions that can be described by mathematical equations.
However, the researchers have made it clear that they have yet not found any evidence that their findings could be extended to other critical aspects of cell behaviour, such as the decisions involved in cell death.
"This pathway, and this decision whether it is time to proliferate, is very tightly coupled to decisions of cell fate. There's a decision as to whether the proliferation process is normal, and if the answer is not, then the result is that the cell dies. We don't know critical dynamics of that process," said Joseph Nevins, a professor of molecular genetics at the Institute for Genome Sciences & Policy.