Fanconi Anemia (FA) is a rare pediatric disease caused by biallelic mutations in any of 19 different genes acting in a common DNA-crosslink repair pathway. FA involves bone marrow failure, hypogonadism, and high risk of hematopoietic and squamous cell cancers. Patient cells exhibit increased chromosome breakage when challenged with a DNA-crosslinking agent such as diepoxybutane (DEB) and show depressed stem cell renewal even in the absence of exogenous DNA damage. To better understand the mechanisms of FA and to facilitate the search for therapeutics, we used insertional mutagenesis and TILLING to generate mutant lines for the FA core-complex genes fancc and fancl, and the downstream gene fancd1(brca2). Zebrafish mutants for all three fanc genes exhibited increased cell death in response to DEB, as well as female-to-male sex reversal and gonadal dysgenesis. While the sex-reversal phenotype is caused by the death of meiotic oocytes in juvenile gonads, little is known about transcriptional changes underlying FA phenotypes during development of whole organisms. Tissues relevant to FA, including hematopoietic tissue, gonads, and the adaptive immune system, all develop in zebrafish in the first month post-fertilization. We used RNA-seq to compare gene expression between FA mutants and wild-type siblings in larval and juvenile zebrafish. We generated strand-specific cDNA libraries from 3-5 replicates of mutant and wild-type zebrafish at 4, 10, 14, 18, 22, 26, and 30 days post-fertilization and sequenced them at an average depth of 20 million reads on an Illumina HiSeq. Differential expression was found in genes involved in mitochondrial function and oxidative stress. These results provide a fuller understanding of the mechanisms of FA disease and may help identify new target genes for human therapies.