"Now we have a better handle on what these proteins do and how a potential drug might affect their activity," said Bernhardt, a co-author of the paper and HMS Professor of Microbiology and Immunobiology.
Cell walls are made of linked chains of sugars and are integral to a cells’ survival. A cell wall can keep out toxins and harmful invaders as well as maintain the shape of form of the cell.
In 1957, researchers discovered that penicillin worked by stopping the proteins that create bacterial cell walls. In the 1970s and 1980s, it was learned how those proteins that penicillin blocks work to build the cell wall. For a time, those proteins were assumed to be the primary drivers of cell wall synthesis in bacteria.
Tsuyoshi Uehara, another co-author and a former HMS research fellow in the Bernhardt lab, had an idea for what the missing enzyme could be - the SEDS (shape, elongation, division and sporulation) family of proteins. The family is poorly characterized, yet known to be critical during cell growth, division and sporulation.
The research team removed all proteins that synthesize the cell wall and are known to bind penicillin; they observed SEDS proteins behaving normally. This indicated to the researchers that they were on the right track.
Further experimentation confirmed their hypothesis that the SEDS proteins are a cell wall synthesizing family. They were also able to demonstrate that the SEDS family builds hoop-like structures around the cell, and the penicillin-binding proteins fill in smaller strands to complete the cell wall.
SEDS proteins are also more common than the proteins that bind penicillin, and that might mean an antibiotic that targeted SEDS proteins could be more effective against a range of bacteria.
Sources: AAAS/Eurekalert! via Harvard Medical School, Nature