The average jump time at key hydration sites (e.g., 2 ′ OH, phosphate O S and O R ) is identical in both sequences within the computed error bars (see SI)). Interestingly, the only significant difference with alternating base pairs is observed at the slow O2(C) on the floor of the DNA minor groove, with an average jump time of 24.4 ± 1.1 ps in GGGG and 31.2 ± 2 ps in GCGC. This sequence dependence of the dynamics at slow sites in the groove is here specific to DNA, which is consistent with previous work. The slow hydration sites, phosphate groups and the floor of narrow grooves are also key interaction sites with ions and proteins, and thus often involved in the formation of protein-nucleic acid complexes and drug binding events. We thus want to go beyond the high-resolution site-level characterization of differences between DNA and RNA hydration dynamics. We now seek a physical understanding of the molecular origin of these differences, focusing on the slow sites and starting with phosphate hydration, where we found distinctly slower hydration dynamics next to phosphate O R sites in RNA. In A-RNA, water molecules have been found to bridge neighbor phosphate groups, and suggested by simulations to form long-lived water bridges. In our simulations, successive phosphate O R oxygen atoms along each strand are indeed bridged by a single water molecule 43% of the time. However, these water bridges are not responsible for the slow hydration dynamics encountered around the phosphate groups, since the jump dynamics of water molecules initially H-bonded to a phosphate O R atom are very similar irrespective of whether the second hydrogen atom is H-bonded to the neighbor phosphate group (bridge conformation) or to water (not bridge) (see SI Fig. ). In other words, the H-bonds formed by a water molecule in bridge between two phosphate groups are not longer lived than those of other water molecules bound to the phosphate O R . This finding nuances the usual picture of long-lived water bridges between RNA phosphates. However, the location of the "bridging" water molecules is much better defined by the 2 H-bonds with the phosphate backbone compared to singly-bound water molecules, which leads to a higher water density at those specific locations and explains their better resolution in X-ray experiments. Since the peculiar slowdown at RNA O R sites is not due to long-lived water bridges, we now use our jump model for water reorientation dynamics to identify the physical determinants of the slowdown next to these sites in DNA and RNA, and understand which physical factors cause the split in water reorientation dynamics between the two phosphate oxygen atoms in RNA. Previous works have shown that the effect of the environment on the jump time can be quantified through two main factors, ρ = ρ T SEV × ρ T SHB (details in SI). The entropic Transition-State Excluded Volume (TSEV) factor, ρ T SEV , quantifies the slowdown due to the presence of a nearby solute that hinders the approach of the new acceptor. The Transition State Hydrogen Bond (TSHB) factor ρ T SHB describes how the nature and restraints imposed by the solute modulate the free energy cost to elongate the initial H-bond to its transition-state geometry.