Hundreds of embryo-lethal loss-of-function mutants have been identified in Arabidopsis and other species. We identified a novel embryo-lethal mutant that resulted in a lack of embryo chlorophyll pigmentation and aberrant cell divisions. Loss-of-function mutant embryos were unable to germinate and develop on soil but were able to on ½ MS media supplemented with 1% sucrose, but produced stunted, albino seedlings. The mutant phenotype was caused by an 8bp deletion in the coding region of the At1g73710 gene encoding a putative pentatricopeptide repeat (PPR) protein. CRISPR-targeted mutations of At1g73710 confirmed causality. The protein is predicted to bind to and regulate the expression of several chloroplast transcripts, that are currently being investigated. DIC microscopy showed that the absence of the PPR led to a range of embryogenesis phenotypes, including aberrant cotyledon development and the premature arrest of embryogenesis. Transmission electron micrographs of leaf tissue showed that the albino phenotype was associated with reduced chloroplast and thylakoid membrane formation in the loss-of-function mutants. Our results indicate that At1g73710 is an RNA-binding PPR protein essential for normal chloroplast and embryo development