Montana State scientists discover backup pathway for cysteine production in mammalian cells

September 24, 2026 at 05:00 AM2 min

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Montana State University geneticist Ed Schmidt and colleagues discovered a previously unknown survival mechanism that allows mammalian cells to produce cysteine when the normal disulfide reductase systems fail. The finding, published in Nature Chemical Biology, overturns a decades-old assumption that at least one functioning disulfide reductase is essential for cellular life. The discovery emerged from genetically engineered mice that survived conditions once considered impossible.

Key Facts

The study was published in Nature Chemical Biology.
The first clue appeared in 2014 when genetically engineered mice lacking any known cysteine-producing disulfide reductase system survived.
The discovery took nine years and unfolded in three stages.
Lead author Ed Schmidt is a professor of genetics and development in the Department of Microbiology and Cell Biology at Montana State University.

Cysteine Dependency

All cells require a constant supply of the amino acid cysteine to stay alive, but cysteine is not available outside the cells. Cysteine is used to make proteins, helps cells protect themselves from damage, and contributes to the formation of disulfide bonds that stabilize protein structures. For decades, researchers believed cells could not obtain cysteine from their surroundings and had to generate it internally by breaking apart cystine, an oxidized form of cysteine. Cells normally accomplish this through a disulfide reductase system, and scientists long assumed that having at least one functioning version of this system was essential for cellular life.

Impossible Survival

The discovery unfolded in three stages over nine years, beginning with a colony of genetically engineered mice that survived under conditions that should have been fatal. The mice lacked any known mechanism for converting cystine into the cysteine their cells required, which was supposed to be impossible. Schmidt had previously engineered mice whose liver cells separately lacked one or the other of the two main disulfide reductases, and their physiological responses led him to question the prevailing assumption. Finding the explanation for the backup pathway took another seven years after the initial 2014 observation.