Missions may be regarded as a narrative for challenge-oriented policies, as a rationale for directional policies, and as an instrument for coordinating distributed innovation efforts. While the attention for mission-oriented innovation policy is rising, there are still many questions regarding both the governance and the conduct of missions as well as the (adverse) effects they might have on innovation and societal challenges. This research perspective reflects on what missions are, what they can do and potentially engender, and how they can be studied empirically. Rather than a static, predetermined, and closed-off instrument, we contend that missions are best understood as continuously interacting with the structures and interests of governments, markets, and society, aligning (1) problem-based governance targeting societal challenges and (2) innovation governance targeting novelty creation and deployment. This characterisation of missions, as embedded and evolving, advances empirical questions that could guide research into unexplored directions.

Recent times have seen the rediscovery and adaptation of mission-oriented innovation policies (MIPs) for driving transformative change. While such policies seek to mobilise and align stakeholders, little is known about how missions feature in policy coordination processes. We argue that to facilitate the still troublesome operationalisation of MIPs, it is essential to understand missions as ‘boundary objects’ that have some shared meanings among the participants they convene, yet are open enough to be interpreted differently by distinct actors gathering in four interconnected policy arenas—i.e. a strategic, programmatic, implementation, and performance arena. By studying the European Commission’s Horizon Europe missions, we unravel how missions as boundary objects enable and disable the coordination of heterogeneous communities. The resulting analytical perspective highlights three key mechanisms for coordinating mission meanings across communities and arenas: convergence–divergence, passage, and reflexive learning. We conclude with research avenues for studying missions as boundary objects for facilitating concerted action.

Autosomal dominant polycystic liver disease (PCLD) is a rare progressive disorder characterized by an increased liver volume due to many (>20) fluid-filled cysts of biliary origin. Disease causing mutations in PRKCSH or SEC63 are found in approximately 25% of the PCLD patients. Both gene products function in the endoplasmic reticulum, however, the molecular mechanism behind cyst formation remains to be elucidated. As part of the translocon complex, SEC63 plays a role in protein import into the ER and is implicated in the export of unfolded proteins to the cytoplasm during ER-associated degradation (ERAD). PRKCSH codes for the beta-subunit of glucosidase II (hepatocystin), which cleaves two glucose residues of Glc(3)Man(9)GlcNAc(2) N-glycans on proteins. Hepatocystin is thereby directly involved in the protein folding process by regulating protein binding to calnexin/calreticulin in the ER. A separate group of genetic diseases affecting protein N-glycosylation in the ER is formed by the congenital disorders of glycosylation (CDG). In distinct subtypes of this autosomal recessive multisystem disease specific liver symptoms have been reported that overlap with PCLD. Recent research revealed novel insights in PCLD disease pathology such as the absence of hepatocystin from cyst epithelia indicating a two-hit model for PCLD cystogenesis. This opens the way to speculate about a recessive mechanism for PCLD pathophysiology and shared molecular pathways between CDG and PCLD. In this review we will discuss the clinical-genetic features of PCLD and CDG as well as their biochemical pathways with the aim to identify novel directions of research into cystogenesis.