Scientists have for the first time uncovered the role played by cyclin – a protein important for cell division – in driving the growth of the malaria parasite in mosquitoes.
The team, from the School of Life Sciences at the University of Nottingham in the UK, reports the findings in the journal PLOS Pathogens.
The researchers believe the discovery will increase understanding of how the malaria parasite thrives inside its insect and human hosts – information that is important for developing treatments to stop the disease.
Every year, malaria spreads to hundreds of millions of people around the world and claims nearly half a million lives. The vast majority of cases and deaths occur in sub-Saharan Africa.
Malaria is caused by a parasite called Plasmodium that spreads to mammals via the bite of infected female mosquitoes. Symptoms include fever, headache and vomiting. They usually appear 10-15 days after the mosquito bite.
Plasmodium has a complex life cycle that requires two hosts: the mosquito and a mammal, such as a human being. In the human body, it multiplies in the liver and infects red blood cells.
If not treated, malaria can quickly disrupt the blood supply to vital organs and become life-threatening.
The single-celled parasite has many features in common with other complex cells, such as yeast cells and human cells. One of these is the way it controls the processes of cell division so they only occur at the right time.
‘First functional study of cyclin in the malaria parasite’
A protein called cyclin plays a key role in the timing and control of cell division. It has been studied in great detail in human, yeast and plant cells, but its function in Plasmodium has not been so clear, say the authors in their paper.
The team identified three types of cyclin in Plasmodium and carried out a detailed analysis of one – a “P-type” called CYC3 that is closely related to cyclins found in plants.
A distinctive feature of Plasmodium is that it undergoes two types of cell division – asexual and sexual. During the asexual process, the chromosomes inside the cell nucleus divide but the nucleus itself does not – this is called “endomitosis.”
Using a species of Plasmodium that infects rats, the researchers showed that deleting CYC3 led to several abnormalities in this unusual type of cell division while the parasite is in the mosquito.
They were also able to identify cell processes important for signaling, host cell invasion and parasite development that appear to rely on CYC3.
Lead author Dr. Magali Roques concludes:
“This first functional study of cyclin in the malaria parasite and its consequences in parasite development within pathogen-carrying mosquitoes will definitely further our understanding of parasite cell division, which I hope will lead to the elimination of this disease in the future.”
Meanwhile, Medical News Today has learned that the fight against malaria could be undermined by relapsing infections rather than new infections. Researchers who ran a clinical trial in Papua New Guinea concluded this could the case in the Asia-Pacific region.