Augmenter of Liver Regeneration (ALR) is a sulfhydryl oxidase carrying out fundamental functions facilitating protein disulfide bond formation. In mammals, it also functions as a hepatotrophic growth factor that specifically stimulates hepatocyte proliferation and promotes liver regeneration after liver damage or partial hepatectomy. Whether ALR also plays a role during vertebrate hepatogenesis is unknown. In this work, we investigated the function of alr in liver organogenesis in zebrafish model. We showed that alr is expressed in liver throughout hepatogenesis. Knockdown of alr through morpholino antisense oligonucleotide (MO) leads to suppression of liver outgrowth while overexpression of alr promotes liver growth. The small-liver phenotype in alr morphants results from a reduction of hepatocyte proliferation without affecting apoptosis. When expressed in cultured cells, zebrafish Alr exists as dimer and is localized in mitochondria as well as cytosol but not in nucleus or secreted outside of the cell. Similar to mammalian ALR, zebrafish Alr is a flavin-linked sulfhydryl oxidase and mutation of the conserved cysteine in the CxxC motif abolishes its enzymatic activity. Interestingly, overexpression of either wild type Alr or enzyme-inactive AlrC131S mutant promoted liver growth and rescued the liver growth defect of alr morphants. Nevertheless, alr C131S is less efficacious in both functions. Meantime, high doses of alr MOs lead to widespread developmental defects and early embryonic death in an alr sequence-dependent manner. These results suggest that alr promotes zebrafish liver outgrowth using mechanisms that are dependent as well as independent of its sulfhydryl oxidase activity. This is the first demonstration of a developmental role of alr in vertebrate. It exemplifies that a low-level sulfhydryl oxidase activity of Alr is essential for embryonic development and cellular survival. The dose-dependent and partial suppression of alr expression through MO-mediated knockdown allows the identification of its late developmental role in vertebrate liver organogenesis.

Adopting the Critical Discourse Analysis perspective, this study investigates the ideology reflected by the anti-Islam and anti-Muslim discourse in China, the power dynamics revealed by such discourse and how social media discourse differs from and utilises the government discourse. Four ways to disguise the anti-Muslims, anti-Islam prejudice are investigated: appealing to patriotism to demand cultural assimilation; claiming to defend secularism; framing Islam as incompatible with mainstream culture; appealing to consumer rights to reject halal food. Non-Muslims and assimilated Muslims (especially the elites) are found to have the prerogative to dictate who belong to the ingroup, what dietary restrictions are legitimate and whom to blame when undesirable situations arise, while Muslim non-elites are at the receiving end of such dictates. This study also argues that social media discourse expresses antagonism of higher intensity than the government discourse does, and may misappropriate the official narratives to express the interlocutor’s hatred towards Muslims.

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