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Credit: Stuart Hay
Scientists believe they have discovered a weak spot in the malaria life cycle that could be exploited to prevent the disease from spreading.
The team found that female malaria parasites take on fat differently than male parasites.
And the protein gABCG2, which controls the transport of fat molecules, plays a key role in malaria parasite survival.
Phuong Tran, PhD, of Australia National University in Canberra, and his colleagues recounted these findings in Nature Communications.
The researchers noted that ATP-binding cassette transporters are known to play key roles in drug resistance. And the genome of the Plasmodium falciparum parasite encodes multiple members of this family, including gABCG2, which is transcribed predominantly in the gametocyte stage.
So the team used gene deletion and tagging to investigate the expression, localization, and function of gABCG2. They found that gABCG2 was only present in female gametocytes—in a single, lipid-like structure.
“Female parasites build a deposit of fat in a localized spot, which is controlled by gABCG2,” said study author Alexander Maier, PhD, of Australia National University.
“However, malaria genetically modified to have no gABCG2 did not accumulate fat in the same way, and crucially, struggled to survive in the mosquito.”
Cell lines in which gABCG2 was knocked out produced more gametocytes of both sexes, but they showed a reduction in cholesteryl esters, diacylglycerols, and triacylglycerols.
The researchers therefore concluded that gABCG2 regulates gametocyte numbers and the accumulation of neutral lipids, which are likely important for parasite development in the insect stages of the parasite life cycle.
Dr Tran said this discovery could lead to new malaria drugs based on current drugs that influence fat digestion.
“If we can target the molecule gABCG2 and kill the females, then we can stop the fertilization, which will stop the development and transmission of the disease,” he said. “It may even lead to a vaccine for malaria.” 
Credit: Stuart Hay
Scientists believe they have discovered a weak spot in the malaria life cycle that could be exploited to prevent the disease from spreading.
The team found that female malaria parasites take on fat differently than male parasites.
And the protein gABCG2, which controls the transport of fat molecules, plays a key role in malaria parasite survival.
Phuong Tran, PhD, of Australia National University in Canberra, and his colleagues recounted these findings in Nature Communications.
The researchers noted that ATP-binding cassette transporters are known to play key roles in drug resistance. And the genome of the Plasmodium falciparum parasite encodes multiple members of this family, including gABCG2, which is transcribed predominantly in the gametocyte stage.
So the team used gene deletion and tagging to investigate the expression, localization, and function of gABCG2. They found that gABCG2 was only present in female gametocytes—in a single, lipid-like structure.
“Female parasites build a deposit of fat in a localized spot, which is controlled by gABCG2,” said study author Alexander Maier, PhD, of Australia National University.
“However, malaria genetically modified to have no gABCG2 did not accumulate fat in the same way, and crucially, struggled to survive in the mosquito.”
Cell lines in which gABCG2 was knocked out produced more gametocytes of both sexes, but they showed a reduction in cholesteryl esters, diacylglycerols, and triacylglycerols.
The researchers therefore concluded that gABCG2 regulates gametocyte numbers and the accumulation of neutral lipids, which are likely important for parasite development in the insect stages of the parasite life cycle.
Dr Tran said this discovery could lead to new malaria drugs based on current drugs that influence fat digestion.
“If we can target the molecule gABCG2 and kill the females, then we can stop the fertilization, which will stop the development and transmission of the disease,” he said. “It may even lead to a vaccine for malaria.”
Credit: Stuart Hay
Scientists believe they have discovered a weak spot in the malaria life cycle that could be exploited to prevent the disease from spreading.
The team found that female malaria parasites take on fat differently than male parasites.
And the protein gABCG2, which controls the transport of fat molecules, plays a key role in malaria parasite survival.
Phuong Tran, PhD, of Australia National University in Canberra, and his colleagues recounted these findings in Nature Communications.
The researchers noted that ATP-binding cassette transporters are known to play key roles in drug resistance. And the genome of the Plasmodium falciparum parasite encodes multiple members of this family, including gABCG2, which is transcribed predominantly in the gametocyte stage.
So the team used gene deletion and tagging to investigate the expression, localization, and function of gABCG2. They found that gABCG2 was only present in female gametocytes—in a single, lipid-like structure.
“Female parasites build a deposit of fat in a localized spot, which is controlled by gABCG2,” said study author Alexander Maier, PhD, of Australia National University.
“However, malaria genetically modified to have no gABCG2 did not accumulate fat in the same way, and crucially, struggled to survive in the mosquito.”
Cell lines in which gABCG2 was knocked out produced more gametocytes of both sexes, but they showed a reduction in cholesteryl esters, diacylglycerols, and triacylglycerols.
The researchers therefore concluded that gABCG2 regulates gametocyte numbers and the accumulation of neutral lipids, which are likely important for parasite development in the insect stages of the parasite life cycle.
Dr Tran said this discovery could lead to new malaria drugs based on current drugs that influence fat digestion.
“If we can target the molecule gABCG2 and kill the females, then we can stop the fertilization, which will stop the development and transmission of the disease,” he said. “It may even lead to a vaccine for malaria.”