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Balanced symmetric and asymmetric divisions of neural progenitor cells (NPCs) are crucial for brain development, but the underlying mechanisms are not fully understood. Here we report that mitotic kinesin KIF20A/MKLP2 interacts with RGS3 and plays a crucial role in controlling the division modes of NPCs during cortical neurogenesis. Knockdown of KIF20A in NPCs causes dislocation of RGS3 from the intercellular bridge (ICB), impairs the function of Ephrin-B–RGS cell fate signaling complex, and leads to a transition from proliferative to differentiative divisions. Germline and inducible knockout of KIF20A causes a loss of progenitor cells and neurons and results in thinner cortex and ventriculomegaly. Interestingly, loss of function of KIF20A induces early cell cycle exit and precocious neuronal differentiation without causing substantial cytokinesis defect or apoptosis. Our results identify a RGS–KIF20A axis in the regulation of cell division and suggest a potential link of the ICB to regulation of cell fate determination.

Level-0 (L0) caches have been proposed in the past as an inexpensive way to improve performance and reduce energy consumption in resource-constrained embedded processors. This paper proposes new L0 data cache organizations using the assumption that an L0 hit/miss determination can be completed prior to the L1 access. This is a realistic assumption for very small L0 caches that can nevertheless deliver significant miss rate and/or energy reduction. The key issue for such caches is how and when to move data between the L0 and L1 caches. The first new cache, a flow cache, targets a conflict miss reduction in a direct-mapped L1 cache. It offers a simpler hardware design and uses on average 10% less dynamic energy than the victim cache with nearly identical performance. The second new cache, a hit cache, reduces the dynamic energy consumption in a set-associative L1 cache by 30% without impacting performance. A variant of this policy reduces the dynamic energy consumption by up to 50%, with 5% performance degradation.

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