Assembly of photosystem II (PSII) occurs sequentially and requires several auxiliary proteins, such as ALB3. Here, we report on the function of the Arabidopsis thaliana thylakoid membrane protein Tellurite Resitance C (AtTerC) in this process. Knockout of AtTerC was previously shown to be seedling lethal. This phenotype could be rescued by expressing TerC fused C-terminally to GFP in the terc-1 background, and the resulting terc-1TerC- GFP line and an artificial miRNA-based knockdown allele (amiR-TerC) were employed to analyze the TerC function. Alteration in chlorophyll fluorescence and in thylakoid ultrastructure observed in amiR-TerC plants and terc-1TerC- GFP were attributed to defects in PSII. We show that this phenotype resulted from a reduction in the rate of de novo synthesis of PSII core proteins, whereas later steps in PSII biogenesis seemed to be less affected. Yeast-two-hybrid assays showed that TerC interacts with PSII proteins. Particular its interaction with the PSII assembly factors ALB3 has been approved by co-immunoprecipitation. ALB3 is thought to assist CP43 assembly into PSII via its interaction with LPA2 and LPA3. Homozygous lpa2 mutants bearing amiR-TerC displayed markedly exacerbated phenotypes, leading to seedling lethality, indicating an additive effect. We propose a model, in which TerC together with ALB3 facilitates de novo synthesis of thylakoid membrane proteins, for instance CP43, at the membrane insertion step. This article is protected by copyright. All rights reserved.