Mercury's interior structure, rotation, and tides

This review addresses the deep interior structure of Mercury. Mercury is thought to consist of similar chemical reservoirs (core, mantle, crust) as the other terrestrial planets, but with a relatively much larger core. Constraints on Mercury’s composition and internal structure are reviewed, and possible interior models are described. Large advances in our knowledge of Mercury’s interior are not only expected from imaging of characteristic surface features but particularly from geodetic observations of the gravity field, the rotation, and the tides of Mercury. The low-degree gravity field of Mercury gives information on the differences of the principal moments of inertia, which are a measure of the mass concentration toward the center of the planet. Mercury’s unique rotation presents several clues to the deep interior. From observations of the mean obliquity of Mercury and the low-degree gravity data, the moments of inertia can be obtained, and deviations from the mean rotation speed (librations) offer an exciting possibility to determine the moment of inertia of the mantle. Due to its proximity to the Sun, Mercury has the largest tides of the Solar System planets. Since tides are sensitive to the existence and location of liquid layers, tidal observations are ideally suited to study the physical state and size of the core of Mercury

HNRNPC haploinsufficiency affects alternative splicing of intellectual disability-associated genes and causes a neurodevelopmental disorder

Heterogeneous nuclear ribonucleoprotein C (HNRNPC) is an essential, ubiquitously abundant protein involved in mRNA processing. Genetic variants in other members of the HNRNP family have been associated with neurodevelopmental disorders. Here, we describe 13 individuals with global developmental delay, intellectual disability, behavioral abnormalities, and subtle facial dysmorphology with heterozygous HNRNPC germline variants. Five of them bear an identical in-frame deletion of nine amino acids in the extreme C terminus. To study the effect of this recurrent variant as well as HNRNPC haploinsufficiency, we used induced pluripotent stem cells (iPSCs) and fibroblasts obtained from affected individuals. While protein localization and oligomerization were unaffected by the recurrent C-terminal deletion variant, total HNRNPC levels were decreased. Previously, reduced HNRNPC levels have been associated with changes in alternative splicing. Therefore, we performed a meta-analysis on published RNA-seq datasets of three different cell lines to identify a ubiquitous HNRNPC-dependent signature of alternative spliced exons. The identified signature was not only confirmed in fibroblasts obtained from an affected individual but also showed a significant enrichment for genes associated with intellectual disability. Hence, we assessed the effect of decreased and increased levels of HNRNPC on neuronal arborization and neuronal migration and found that either condition affects neuronal function. Taken together, our data indicate that HNRNPC haploinsufficiency affects alternative splicing of multiple intellectual disability-associated genes and that the developing brain is sensitive to aberrant levels of HNRNPC. Hence, our data strongly support the inclusion of HNRNPC to the family of HNRNP-related neurodevelopmental disorders