AP Biology class blog for discussing current research in Biology

Author: matosis

Deleting Genes to Stop Malaria

A new discovery has highlighted the positive effects that the revolutionary new gene editing tool, CRISPR-Cas9, can have. Scientists at the Johns Hopkins Bloomberg School of Public Health’s Malaria Research Institute have discovered that the deletion of a single gene from the Anopheles Gambiae mosquito, called the FREP1 gene, yields promising results in the eradication of the malaria disease.


Image result for mosquito gene editing

Gene Editing

The FREP1 gene has been associated with being a malaria “host factor” gene because it helps the parasite live in the gut of the mosquitoes.  However, the scientists, using the CRISPR-Cas9 gene editing procedures, have been able to delete the FREP1 gene from the mosquitoes and have seen significant decreases in the spread of malaria. Without the host factor gene, the parasite has difficulty surviving in the mosquito, which decreases the spread of the disease to other organisms.


The deletion of the FREP1 gene had other effects in addition to the resistance of the malaria parasites. In the mosquitoes where the gene was deleted, many showed no signs of sporozoite-stage parasites in their salivary glands, which can spread to humans through mosquito bites. George Dimopoulos, PhD, professor in the Bloomberg School’s Department of Molecular Microbiology and Immunology, commented on the study, saying that “if you could successfully replace ordinary, wild-type mosquitoes with these modified mosquitoes, it’s likely that there would be a significant impact on malaria transmission”.

Beetle and Bacteria are Best of Friends

The thistle tortoise beetle, a type of insect native to Eurasia, has, astonishingly, the ability to break down pectin.  Pectin is a polysaccharide that makes up plant cell walls that is undigestable to most animals due to its structure.  The tortoise beetle, a leaf-eater, has developed a symbiotic relationship with a certain bacteria that can break down pectin, allowing the leaf-munching insects to chow away.

Thistle Tortoise Beetle

Hassan Salem, the lead author of the study, became interested in how the small insects had the ability to gain nutrients from plant cell walls.  Salem looked in the gut of the beetle and noticed a certain bacteria with the genes to create enzymes that allow pectin and other tough molecules to be broken down in the beetle, where the beetle’s digestive tract can then absorb the nutrients.  What makes the bacteria interesting is that it contains significantly fewer DNA base pairs in its genome.  A typical bacteria has millions of DNA base pairs while this bacteria only has around 270,000 DNA base pairs.

Thistle Tortoise Beetle on a leaf

The bacteria has developed such an advantageous symbiotic relationship with the thistle tortoise beetle that it doesn’t require an abundance of DNA base pairs.  The strain of bacterium is more similar to that of “intracellular bacteria and organelles than to free-living bacteria” (Clark).  The bacteria is so important to the survival of the beetle that female beetles insert a portion of their own bacteria into each egg so that the unhatched insects can create their own colonies.  Salem named the bacteria Candidatus Stammera capleta.

Learn From the Greeks: The “Trojan Horse” Method to Cure Ebola

The study to find a cure for the dangerous virus Ebola has resulted in a promising new find: a new strategy has shown positive results.  This new technique involves the placement of antibodies into the cell with the Ebola virus and then it binds to the NPC1 protein before the virus can, essentially rendering it useless.

To understand exactly how these special rainbow unicorn antibodies work, it is essential if we know how the Ebola virus spreads.  The different strains of the Ebola virus (Sudan, Zaire, Tai Forest, Bundibugyo, and Reston) are genetically a little different but they do the same thing.  The virus enters the cell through glycoproteins and gets engulfed into a lysosome. Once inside a lysosome, the virus transforms into a new state where it can bind to a human protein called NPC1.  Once bound to this protein the virus can eject its information into the cytoplasm of the cell and spread.

The solution lies in the binding of the special antibody.  The antibody ZMapp can effectively destroy the Ebola virus, but it is only effective on the Zaire strain. The other strains of Ebola are a little genetically different that the ZMapp antibody does not detect the other strains. Thus, a different approach is required to fight the virus.  The virus can be stopped if an antibody is able to enter the cell with the virus and either bind to the NPC1 protein before the virus does or bind to the virus to disable its ability to bind to anything else.

When the Ebola virus is in a cell’s lysosome it structurally alters itself to enable it to bind with the NPC1, and an advantage that scientists have discovered is that between the different strains of Ebola virus, the transformed versions are very similar, thus an antibody can be made that can bind to all of the different strains.  The problem with this, however, is that antibodies cannot enter the cell the same way that viruses can.

Ebola Virus

The solution that the researchers came up with stems back to the Trojan Horse story from Ancient Greece. The researchers added an extra arm to the antibody, enabling it to latch onto the virus and hitch a ride with it into the lysosome.  Once in the lysosome with the virus, the virus alters and the antibody can then bind again and disable the virus.  This method can potentially be a cure for all of the strains of the Ebola virus, causing an end to a very dangerous virus.

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