Follistatin like-1 ( <i>Fstl1</i> ) regulates adipose tissue development in zebrafish

Obesity is a highly prevalent disorder with complex aetiology. Therefore, studying its associated cellular and molecular pathways may be aided by analysing genetic tractable diseases. In this context, the study of ciliopathies such as Bardet-Biedl syndrome has highlighted the relevance of primary cilia in obesity, both in the central nervous system and peripheral tissues. Based on our previous <i>in vitro</i> results supporting the role of a novel Bbs4-cilia-Fstl1 axis in adipocyte differentiation, we evaluated the <i>in vivo</i> relevance of the zebrafish orthologous genes <i>fstl1a</i> and <i>fstl1b</i> in primary cilia and adipose tissue development. Using a combination of knockdowns and a new <i>fstl1a</i> mutant line, we show that <i>fstl1a</i> promotes primary cilia formation in early embryos and participates in adipose tissue formation in larvae. We also show that <i>fstl1b</i> partially compensates for the loss of <i>fstl1a</i>. Moreover, in high fat diet, <i>fstl1a</i> depletion affects the expression of differentiation and mature adipocyte markers. These results agree with our previous <i>in vitro</i> data and provide further support for the role of FSTL1 as a regulator of adipose tissue formation. Dissecting the exact biological role of proteins such as FSTL1 will likely contribute to understand obesity onset and presentation.