We run self-consistent simulations of Milky Way-sized, isolated disk galaxies to study formation and evolution of a stellar bar as well as a nuclear ring in the presence of gas. We consider two sets of models with cold or warm disks that differ in the radial velocity dispersions, and vary the gas fraction f gas by fixing the total disk mass. A bar forms earlier and more strongly in the cold disks with larger f gas , while gas progressively delays the bar formation in the warm disks . The bar formation enhances a central mass concentration which in turn makes the bar decay temporarily, after which it regrows in size and strength, eventually becoming stronger in models with smaller f gas . Although all bars rotate fast in the beginning, they rapidly turn to slow rotators. In our models, only the gas-free, warm disk undergoes rapid buckling instability, while other disks thicken more gradually via vertical heating. The gas driven inward by the bar potential readily forms a star-forming nuclear ring. The ring is very small when it first forms and grows in size over time. The ring star formation rate is episodic and bursty due to feedback, and well correlated with the mass inflow rate to the ring. Some expanding shells produced by star formation feedback are sheared out in the bar regions and collide with dust lanes to appear as filamentary interbar spurs. The bars and nuclear rings formed in our simulations have properties similar to those in the Milky Way.

Nuclear rings in barred galaxies are sites of active star formation. We use hydrodynamic simulations to study temporal and spatial behavior of star formation occurring in nuclear rings of barred galaxies where radial gas inflows are triggered solely by a bar potential. The star formation recipes include a density threshold, an efficiency, conversion of gas to star particles, and delayed momentum feedback via supernova explosions. We find that star formation rate (SFR) in a nuclear ring is roughly equal to the mass inflow rate to the ring, while it has a weak dependence on the total gas mass in the ring. The SFR typically exhibits a strong primary burst followed by weak secondary bursts before declining to very small values. The primary burst is associated with the rapid gas infall to the ring due to the bar growth, while the secondary bursts are caused by re-infall of the ejected gas from the primary burst. While star formation in observed rings persists episodically over a few Gyr, the duration of active star formation in our models lasts for only about a half of the bar growth time, suggesting that the bar potential alone is unlikely responsible for gas supply to the rings. When the SFR is low, most star formation occurs at the contact points between the ring and the dust lanes, leading to an azimuthal age gradient of young star clusters. When the SFR is large, on the other hand, star formation is randomly distributed over the whole circumference of the ring, resulting in no apparent azimuthal age gradient. Since the ring shrinks in size with time, star clusters also exhibit a radial age gradient, with younger clusters found closer to the ring. The cluster mass function is well described by a power law, with a slope depending on the SFR. Giant gas clouds in the rings have supersonic internal velocity dispersions and are gravitationally bound.

Estrogen receptor α (ERα) plays critical roles in development and progression of breast cancer, and the coiled-coil co-activator (CoCoA) is an important ERα co-activator for estrogen-induced gene expression. The small ubiquitin-like modifier (SUMO) pathway is hyperactivated in breast cancer, but the mechanism by which SUMOylation regulates ERα-mediated transcription remains poorly understood. Here, we identified ZFP282 as a CoCoA binding protein. ZFP282 associates directly with ERα and cooperates synergistically with CoCoA to enhance ERα function. ZFP282 is required for estrogen-induced expression of ERα target genes and estrogen-dependent breast cancer cell growth and tumorigenesis. In addition, we found that ZFP282 is SUMOylated and that SUMOylation positively regulates the co-activator activity of ZFP282 by increasing its binding affinity to ERα and CoCoA and consequently increasing recruitment of ZFP282-CoCoA complex to the promoter of ERα target genes. These findings reveal essential roles for ZFP282 and its SUMOylation in estrogen signaling and breast tumorigenesis.