Significance Microalgae accumulate valuable compounds under conditions adverse to growth. For example, nutrient starvation causes accumulation of triacylglycerols but also induces cellular quiescence, characterized by the reversible cessation of growth. Among other factors, this inverse relationship between biomass productivity and triacylglycerol accumulation has long hampered efforts toward the efficient generation of biofuel feedstocks from microalgae. The discovery of a mutant and corresponding protein of Chlamydomonas reinhardtii affecting the orderly transition of algal cells from quiescence to normal growth provides mechanistic insights to address this problem. Quiescent cells also are found in plants and animals. Thus, understanding how Chlamydomonas CHT7 affects the exit out of quiescence promises to provide important insights into the regulation of cellular behavior in multicellular organisms as well. Microalgae are prolific photosynthetic organisms that have the potential to sustainably produce high-value chemical feedstocks. However, an industry based on microalgal biomass still is faced with challenges. For example, microalgae tend to accumulate valuable compounds, such as triacylglycerols, only under stress conditions that limit growth. To investigate the fundamental mechanisms at the base of this conundrum—the inverse relationship between biomass production and storage compound accumulation—we applied a combination of cell biological and genetic approaches. Conceptually, nutrient deprivation, which commonly is used to induce the accumulation of triacylglycerol in microalgae, leads to a state of cellular quiescence defined by a halt of cell divisions that is reversible upon nutrient resupply. To identify factors that govern cellular quiescence, we screened for mutants of the model alga Chlamydomonas reinhardtii that, in contrast to wild-type cells placed under conditions of nitrogen deprivation, were unable to degrade triacylglycerols following nitrogen resupply. One of the mutants described here in detail, compromised hydrolysis of triacylglycerols 7 ( cht7 ), was severely impaired in regrowth following removal of different conditions inducing cellular quiescence. The mutant carries a deletion affecting four genes, only one of which rescued the quiescence phenotype when reintroduced. It encodes a protein with similarity to mammalian and plant DNA binding proteins. Comparison of transcriptomes indicated a partial derepression of quiescence-related transcriptional programs in the mutant under conditions favorable to growth. Thus, CHT7 likely is a repressor of cellular quiescence and provides a possible target for the engineering of high-biomass/high-triacylglycerol microalgae.