Is there such thing as 'populist constitutionalism'? : the case of Hungary

First online: 06 February 2018The paper deals with recent deviations from the shared values of constitutionalism towards a kind of 'populist, illiberal constitutionalism' introduced by Hungary's new constitution in 2011. The populism of FIDESZ was directed against all elites, including the ones that designed the 1989 constitutional system (in which FIDESZ also participated), claiming that it was time for a new revolution. This is why PM Viktor Orban characterized the results of the 2010 elections as a 'revolution of the ballot boxes'. His intention with this revolution was to eliminate all checks and balances, and even the parliamentary rotation of governing parties. His vision for a new constitutional order-one in which his political party occupies the centre stage of Hungarian political life and puts an end to debates over values-has now been entrenched in the new constitution. The paper argues that this current Hungarian constitutional system was made possible by FIDESZ' anti-pluralist nationalist populism, but is not necessarily based on a true commitment to expressing the will of the people via 'illiberal constitutionalism'. The populist government rather misuses the country's lack of constitutional culture. Adherence to constitutional patriotism would mean that FIDESZ would have to endorse what John Rawls once called 'constitutional essentials'. The core of this kind of constitutional patriotism is a constitutional culture centred on universalist liberal democratic norms and values. Instead, the current Hungarian constitutional system is confronted with unconstitutional patriotism, a kind of nationalism that violates constitutional essentials in the name of 'national constitutional identity'

De novo missense variants in phosphatidylinositol kinase PIP5KIγ underlie a neurodevelopmental syndrome associated with altered phosphoinositide signaling

Phosphoinositides (PIs) are membrane phospholipids produced through the local activity of PI kinases and phosphatases that selectively add or remove phosphate groups from the inositol head group. PIs control membrane composition and play key roles in many cellular processes including actin dynamics, endosomal trafficking, autophagy, and nuclear functions. Mutations in phosphatidylinositol 4,5 bisphosphate [PI(4,5)P2] phosphatases cause a broad spectrum of neurodevelopmental disorders such as Lowe and Joubert syndromes and congenital muscular dystrophy with cataracts and intellectual disability, which are thus associated with increased levels of PI(4,5)P2. Here, we describe a neurodevelopmental disorder associated with an increase in the production of PI(4,5)P2 and with PI-signaling dysfunction. We identified three de novo heterozygous missense variants in PIP5K1C, which encodes an isoform of the phosphatidylinositol 4-phosphate 5-kinase (PIP5KIγ), in nine unrelated children exhibiting intellectual disability, developmental delay, acquired microcephaly, seizures, visual abnormalities, and dysmorphic features. We provide evidence that the PIP5K1C variants result in an increase of the endosomal PI(4,5)P2 pool, giving rise to ectopic recruitment of filamentous actin at early endosomes (EEs) that in turn causes dysfunction in EE trafficking. In addition, we generated an in vivo zebrafish model that recapitulates the disorder we describe with developmental defects affecting the forebrain, including the eyes, as well as craniofacial abnormalities, further demonstrating the pathogenic effect of the PIP5K1C variants. We describe a neurodevelopmental disorder associated with de novo gain-of-function variants in PIP5KIγ kinase. The variants cause perturbed endosomal function resulting from increased production of phosphatidylinositol 4,5 bisphosphate and enhanced association of F-actin at endosomes. Moreover, mutant zebrafish larvae recapitulate the phenotypes observed in affected individuals from our cohort