Lon plays the chaperone

Stress placed on the ER is transmitted to mitochondria, but according to new results from Hori et al. on page 1151, protective responses are also sent along. Their results are the first demonstration of a signaling pathway from the ER to mitochondria to initiate adaptive changes that support cellular respiration when protein synthesis is disturbed.

Certain cellular stresses, such as low oxygen or disturbance of Ca²⁺ levels, cause the accumulation of unfolded proteins in the ER. To limit the load on the ER, cytoplasmic protein synthesis is reduced and protein degradation rates increase. However, transcription and translation of several stress responsive genes increase. Hori's group has identified a mitochondrial ATP-dependent protease, Lon, as one such stress-induced gene.

Lon supports mitochondrial function by facilitating assembly of essential mitochondrial proteins. ER stress caused a...