MSU-DOE Plant Research Laboratory, Michigan State University, East Lansing, United States; Department of Plant Biology, Michigan State University, East Lansing, United States
Oliver L Tessmer
MSU-DOE Plant Research Laboratory, Michigan State University, East Lansing, United States
Jacob Bibik
MSU-DOE Plant Research Laboratory, Michigan State University, East Lansing, United States
Nicole Norris
MSU-DOE Plant Research Laboratory, Michigan State University, East Lansing, United States
Eric Pollner
MSU-DOE Plant Research Laboratory, Michigan State University, East Lansing, United States
Ben Lucker
MSU-DOE Plant Research Laboratory, Michigan State University, East Lansing, United States
Sarathi M Weraduwage
MSU-DOE Plant Research Laboratory, Michigan State University, East Lansing, United States; Great Lakes Bioenergy Research Center, Michigan State University, East Lansing, United States
Alecia Withrow
Center for Advanced Microscopy, Michigan State University, East Lansing, United States
Barbara Sears
MSU-DOE Plant Research Laboratory, Michigan State University, East Lansing, United States
Greg Mogos
MSU-DOE Plant Research Laboratory, Michigan State University, East Lansing, United States
Melinda Frame
Center for Advanced Microscopy, Michigan State University, East Lansing, United States
David Hall
MSU-DOE Plant Research Laboratory, Michigan State University, East Lansing, United States
Joseph Weissman
Corporate Strategic Research, ExxonMobil, Annandale, United States
In algae, it is well established that the pyrenoid, a component of the carbon-concentrating mechanism (CCM), is essential for efficient photosynthesis at low CO2. However, the signal that triggers the formation of the pyrenoid has remained elusive. Here, we show that, in Chlamydomonas reinhardtii, the pyrenoid is strongly induced by hyperoxia, even at high CO2 or bicarbonate levels. These results suggest that the pyrenoid can be induced by a common product of photosynthesis specific to low CO2 or hyperoxia. Consistent with this view, the photorespiratory by-product, H2O2, induced the pyrenoid, suggesting that it acts as a signal. Finally, we show evidence for linkages between genetic variations in hyperoxia tolerance, H2O2 signaling, and pyrenoid morphologies.