Anaphase chromosome movement is thought to be mediated by pulling forces generated by end-on attachment of microtubules to the outer face of kinetochores. However, it has been suggested that during C. elegans female meiosis, anaphase is mediated by a kinetochore-independent pushing mechanism with microtubules only attached to the inner face of segregating chromosomes. We found that the kinetochore proteins KNL-1 and KNL-3 are required for preanaphase chromosome stretching, suggesting a role in pulling forces. In the absence of KNL-1,3, pairs of homologous chromosomes did not separate and did not move toward a spindle pole. Instead, each homolog pair moved together with the same spindle pole during anaphase B spindle elongation. Two masses of chromatin thus ended up at opposite spindle poles, giving the appearance of successful anaphase.

Cargo sorting and membrane carrier initiation in recycling endosomes require appropriately coordinated actin dynamics. However, the mechanism underlying the regulation of actin organization during recycling transport remains elusive. Here we report that the loss of PTRN-1/CAMSAP stalled actin exchange and diminished the cytosolic actin structures. Furthermore, we found that PTRN-1 is required for the recycling of clathrin-independent cargo hTAC-GFP The N-terminal calponin homology (CH) domain and central coiled-coils (CC) region of PTRN-1 can synergistically sustain the flow of hTAC-GFP We identified CYK-1/formin as a binding partner of PTRN-1. The N-terminal GTPase-binding domain (GBD) of CYK-1 serves as the binding interface for the PTRN-1 CH domain. The presence of the PTRN-1 CH domain promoted CYK-1-mediated actin polymerization, which suggests that the PTRN-1-CH:CYK-1-GBD interaction efficiently relieves autoinhibitory interactions within CYK-1. As expected, the overexpression of the CYK-1 formin homology domain 2 (FH2) substantially restored actin structures and partially suppressed the hTAC-GFP overaccumulation phenotype in mutants. We conclude that the PTRN-1 CH domain is required to stimulate CYK-1 to facilitate actin dynamics during endocytic recycling.

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Technology of multi-sensor information fusion is an emerging discipline and its theories and methods have been applied in many research areas. In this paper, the model and structure of multi-sensor information fusion, major technologies and methods of information fusion, theoretical system of information fusion as well as application of information fusion technology are introduced and summarized.