The Golgi complex is a processing centre within the biosynthetic secretory pathway, essential for the delivery and production of functional extracellular matrix (ECM), including collagen and proteoglycans. Those large cargoes present a challenge for cells to achieve proper secretion and incorporation into the extracellular matrix, especially during embryonic development. Golgi matrix protein giantin (golgb1) resides at the Golgi rims and here it is considered to participate in secretory cargo traversing through the Golgi complex. Functional knockout of giantin in rodent model systems show considerably different phenotypes depending on the model used. The giantin knockout rats suffer severe osteochondrodysplasia in the head and limbs as well as systemic oedema, whereas knockout mice show milder defects, notably a cleft palate. Previous work in vitro showed that depletion of GOLGB1 by RNAi disrupts ciliogenesis and control of cilium length. In this study, I sought to find an explanation for why loss of giantin causes a cilia defect in vitro and craniofacial defects in vivo. I performed loss-of-function experiments in the zebrafish, using both morpholino and genome engineering techniques targeting giantin. These showed in both instances to affect cilia, craniofacial lay out, and cartilaginous ECM deposition. However, giantin mutants show considerably milder phenotypes than knockdowns. An in vitro giantin knockout cell line displayed compensation as well, cilia number and length were normal. The cause of these acute versus long term loss of giantin discrepancies were investigated by an unbiased RNA sequencing experiment. Data generated from this experiment is pointing towards remodelling of the ECM via transcriptional fine tuning of glycosylation enzymes, proteoglycans such as biglycan, and procollagens. I focussed on GALNT3, a O-glycosylation enzyme, and the small proteoglycan biglycan. Human mutations in GALNT3 lead to tumoral calcinosis, a pathology where patients develop ectopic calcium deposits near joints. Ectopic calcium depositions were also seen in adult giantin mutant fish, which also have reduced levels of galnt3 expression. In vitro, giantin knockout leads to a near loss of GALNT3 in the Golgi complementing zebrafish findings. I also show that the collagen adaptor biglycan is highly abundant in a giantin loss of function setting, suggesting altered collagen deposition and remodelling of the ECM. These findings are pointing towards an ECM adjustment as the dominant response to compensate for chronic depletion of giantin.