Diagnosing Highly-Parallel OpenMP Programs with Aggregated Grain Graphs

Grain graphs simplify OpenMP performance analysis by visualizing performance problems from a fork-join perspective that is familiar to programmers. However, when programmers decide to expose a high amount of parallelism by creating thousands of task and parallel for-loop chunk instances, the resulting grain graph becomes large and tedious to understand. We present an aggregation method that hierarchically groups related nodes together to reduce grain graphs of any size to one single node. This aggregated graph is then navigated by progressively uncovering groups and following visual clues that guide programmers towards problems while hiding non-problematic regions. Our approach enhances productivity by enabling programmers to understand problems in highly-parallel OpenMP programs with less effort than before.acceptedVersionThis is a post-peer-review, pre-copyedit version of an article published in [Lecture Notes in Computer Science] Locked until 1.8.2019 due to copyright restrictions. The final authenticated version is available online at: https://doi.org/10.1007/978-3-319-96983-1_

DNA-PK-Dependent RPA2 Hyperphosphorylation Facilitates DNA Repair and Suppresses Sister Chromatid Exchange

Hyperphosphorylation of RPA2 at serine 4 and serine 8 (S4, S8) has been used as a marker for activation of the DNA damage response. What types of DNA lesions cause RPA2 hyperphosphorylation, which kinase(s) are responsible for them, and what is the biological outcome of these phosphorylations, however, have not been fully investigated. In this study we demonstrate that RPA2 hyperphosphorylation occurs primarily in response to genotoxic stresses that cause high levels of DNA double-strand breaks (DSBs) and that the DNA-dependent protein kinase complex (DNA-PK) is responsible for the modifications in vivo. Alteration of S4, S8 of RPA2 to alanines, which prevent phosphorylations at these sites, caused increased mitotic entry with concomitant increases in RAD51 foci and homologous recombination. Taken together, our results demonstrate that RPA2 hyperphosphorylation by DNA-PK in response to DSBs blocks unscheduled homologous recombination and delays mitotic entry. This pathway thus permits cells to repair DNA damage properly and increase cell viability