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Pathogens often hijack their hosts' cellular proteins in order to get into cells or hide from host immune systems. And at least one pathogen, researchers reveal, can commandeer a whole cellular organelle, taking advantage of it to provide essential building blocks for growth. Thomas Meyer, a molecular biologist at the Max Planck Institute for Infection Biology in Berlin, and his colleagues pursued the question of how pathogens acquire the lipids they need to survive and replicate. On page 731, the authors detail the takeover of a human organelle by the bacterium Chlamydia trachomatis. The bacterium's presence in host cells induces a particular protein to split in two, causing the Golgi apparatus — an organelle comprising membranous stacks that, among other things, generates and sorts lipids — to break down into smaller functional fragments, or 'ministacks'. The pathogen then recruits the ministacks and feeds on their lipids. Meyer tells Nature more.

Why not focus on the bacterium itself rather than its interactions with host cells?

Unlike some other bacteria, Chlamydia is not genetically amenable — we cannot manipulate it as we can Escherichia coli, by generating mutants. So instead of focusing on the bacterial side, we looked to the role of the host cell in the infection process.

How does Chlamydia recruit the ministacks?

That's a mechanism we don't yet understand. During observation, we saw the Golgi break down and the ministacks assemble around the Chlamydia. This recruitment seemed to lead to enhanced transfer of lipids through the membrane surrounding the Chlamydia and into the bacteria.

Does your discovery have implications for the treatment of Chlamydia in humans?

It might open up new avenues for therapeutic approaches, because we now know that the pathogen is not the only potential target for antibiotics. We could, for example, use the host-cell functions a pathogen relies on as drug targets.

How might that work?

When we knocked down expression of Golgi protein genes, we were surprised to find that, rather than being inhibited, Chlamydia replication was boosted. This made sense later when we found that the knockdown caused Golgi fragmentation. In treating this disease, you wouldn't block the genes that are identified in this paper because you would possibly increase replication. You would target other genes that would keep the Golgi intact.