AbstractThe major chlorophyll a/b light harvesting complex (LHCII) of mesophyll chloroplasts is normally assembled late during chloroplast morphogenesis. LHCII occurs at greatly reduced levels in bundle sheath chloroplasts of maize. In order to understand the normal regulatory mechanisms we are examining nuclear maize mutants that alter either (1) the assembly timing or (2) the steady state level of LHCII in mature mesophyll thylakoids. We have found a delayed greening mutant, v24 (on chromosome arm 2L), that unmasks a second unlinked locus, Mof*, that can mediate LHCII assembly timing. The polypeptides of LHCII are encoded by the nuclear multigene cab family. We find that two alleles at Mof* regulate the steady state level of cab mRNA in parallel to their effect on LHCII assembly timing: The genotype Mof*‐1 Mof*‐1 v24 v24 corresponds to reduced cab mRNA and late LHCII assembly timing, while Mof*‐2 Mof*‐2 v24 v24 corresponds to reduced cab mRNA and late LHCII assembly timing. A second group of mutations (Oy‐700, pg11 and pg12 reduces LHCII levels in mesophyll thylakoids. This is the first report that pg11 and pg12) reduce the LHCII of mesophyll thylakoids. The basis of pg11 and pg12 is unknown. Mutations at the Oy locus block the chlorophyll biosynthetic enzyme, protopor‐phyrin IX Mg‐chelatase. Heterozygotes of the codominant mutation Oy‐700 with the normal allele (Oy) have reduced LHCII. We have defined genetic backgrounds that suppress and those that do not suppress the Oy‐700 Oy phenotype under certain conditions: (1) reduced light intensities (200 μE cm−2 sec−1) and/or (2) plant maturity.