Inserting an ultrathin low-conductivity interlayer between the absorber and transport layer has emerged as an important strategy for reducing surface recombination in the best perovskite solar cells. However, a challenge with this approach is a trade-off between the open-circuit voltage ( V oc ) and the fill factor (FF). Here, we overcame this challenge by introducing a thick (about 100 nanometers) insulator layer with random nanoscale openings. We performed drift-diffusion simulations for cells with this porous insulator contact (PIC) and realized it using a solution process by controlling the growth mode of alumina nanoplates. Leveraging a PIC with an approximately 25% reduced contact area, we achieved an efficiency of up to 25.5% (certified steady-state efficiency 24.7%) in p-i-n devices. The product of V oc × FF was 87.9% of the Shockley-Queisser limit. The surface recombination velocity at the p-type contact was reduced from 64.2 to 9.2 centimeters per second. The bulk recombination lifetime was increased from 1.2 to 6.0 microseconds because of improvements in the perovskite crystallinity. The improved wettability of the perovskite precursor solution allowed us to demonstrate a 23.3% efficient 1-square-centimeter p-i-n cell. We demonstrate here its broad applicability for different p-type contacts and perovskite compositions.

Chromosome movements in mitosis are orchestrated by dynamic interactions between spindle microtubules and the kinetochore, a multiprotein complex assembled onto centromeric DNA of the chromosome. Here we show that phosphorylation of human HsMis13 by Aurora B kinase is required for functional kinetochore assembly in HeLa cells. Aurora B interacts with HsMis13 in vitro and in vivo. HsMis13 is a cognate substrate of Aurora B, and the phosphorylation sites were mapped to Ser-100 and Ser-109. Suppression of Aurora B kinase by either small interfering RNA or chemical inhibitors abrogates the localization of HsMis13 but not HsMis12 to the kinetochore. In addition, non-phosphorylatable but not wild type and phospho-mimicking HsMis13 failed to localize to the kinetochore, demonstrating the requirement of phosphorylation by Aurora B for the assembly of HsMis13 to kinetochore. In fact, localization of HsMis13 to the kinetochore is spatiotemporally regulated by Aurora B kinase, which is essential for recruiting outer kinetochore components such as Ndc80 components and CENP-E for functional kinetochore assembly. Importantly, phospho-mimicking mutant HsMis13 restores the assembly of CENP-E to the kinetochore, and tension developed across the sister kinetochores in Aurora B-inhibited cells. Thus, we reason that HsMis13 phosphorylation by Aurora B is required for organizing a stable bi-oriented microtubule kinetochore attachment that is essential for faithful chromosome segregation in mitosis.The kinetochore is a super-molecular complex assembled at each centromere in eukaryotes. It provides a chromosomal attachment point for the mitotic spindle, linking the chromosome to the microtubules and functions in initiating, controlling, and monitoring the movements of chromosomes during mitosis. The kinetochore of animal cells contains two functional domains; that is, the inner kinetochore, which is tightly and persistently associated with centromeric DNA sequences throughout the cell cycle and the outer kinetochore which is composed of many dynamic protein complexes that interact with microtubules only during mitosis. The stable propagation of eukaryotic cells requires each chromosome to be accurately duplicated and faithfully segregated. During mitosis, attaching, positioning, and bi-orientating kinetochores with the spindle microtubules play critical roles in chromosome segregation and genomic stability (see Refs. 1 and 2).Mitosis is orchestrated by signaling cascades that coordinate mitotic processes and ensure accurate chromosome segregation. The key switch for the onset of mitosis is the archetypal cyclin-dependent kinase Cdk1. In addition to the master mitotic kinase Cdk1, three other protein serine/threonine kinase families are also involved, including the Polo kinases, Aurora kinases, and the NEK 3 (NIMA-related kinases) (e.g. Refs. 3 and 4). Recent studies have demonstrated the involvement of NEK kinase in stabilization of the kinetochore-microtubule attachment (e.g. Ref. 5) and the critical role of Aurora B kinase in kineto...

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