Deciphering the genetic determinants involved in cell wall assembly is a strategic issue for breeding programs that target both ruminant feeding and biofuel production. The Arabidopsis thaliana model system has great potentials to elucidate the genetic determinants involved in cell wall component biosynthesis and those involved in the regulation cascades allowing their coordinated assembly. QTL for biomass quality related traits (cell wall content, lignin content, and cell wall degradability) were mapped in the three Arabidopsis RIL progenies Bay0 × Shahdara, Bur0 × Col0, and Blh1 × Col0. Overall, 40 QTL were detected for these traits, explaining up to 33 and 12% of the observed phenotypic variation for lignin content and cell wall degradability respectively. Major QTL hotspots were mapped on chromosome 1 (position 5 Mbp), chromosome 4 (position 1 Mbp), and chromosome 5 (position 3 Mbp). A putative candidate gene set (82 genes) was considered including those previously described as involved in cell wall phenolic component biosynthesis, their regulation factors, and genes involved in lignified tissue patterning. Colocalisations observed (according to the reference sequence of Col0) between the detected QTL and these candidate genes did not prioritize any of the three gene groups (monolignol biosynthesis, transcription factors, lignified tissue patterning). Colocalizations were thus observed for 57% of monolignol biosynthesis related genes, 55% of the transcription factors considered, and 66% of genes considered to be involved in lignified tissue patterning and assembly. Colocalizations were observed for at least one member of all investigated gene families, except WRKY transcription factors. Colocalizations were also shown with several miRNA putatively involved in the regulation of lignifying tissue assembly. Taking into account the QTL shown in the Bur0 × Col0 progeny, allelic variations were shown in the MYB32, MYB58, MYB75, GRAS SCARECROW, AtC3H14 zinc finger, SHINE2, and IFL1 genes and in the AtMIR397a. Given that the list of candidate genes is not complete, and because the QTL support intervals encompassed genes of still unknown function, it is still not clear whether one of the selected candidates is responsible for the effect of a detected QTL. Mutant investigation and positional cloning steps are likely essential to clearly determine the causal mechanism involved in cell wall degradability variation.