Recombination and segregation of chromosomes in meiosis depend critically on the proper assembly and disassembly of the synaptonemal complex (SC), a protein polymer that links homologous chromosomes together. The SC is composed of axial elements localizing to each homologous chromosome, including the HORMA domain-containing protein HTP-1, and central elements localizing between the axial elements. During meiotic prophase in Caenorhabditis elegans, each pair of homologous chromosomes acquires a single off-centered crossover designation site. This crossover location divides the chromosome into two distinct regions of unequal length referred to as the long arm and the short arm. After crossover designation, HTP-1 disassembles from the short arm of the chromosome but persists at the long arm region, as part of a process known as chromosome partitioning (Martinez-Perez et al., 2008). Restriction of HTP-1 to the long arm of the chromosome locally antagonizes the Aurora Kinase homolog AIR-2 (Ferrandiz et al., 2018), which in turn is restricted to the short arm region of partitioned chromosomes. Improper chromosome partitioning and AIR-2 restriction defects can lead to inadequate chromosome segregation. In other organisms, the AAA+ ATPase Pch2/TRIP13 is able to disassemble HORMA domain proteins from the synaptonemal complex during meiosis (Wojtasz et al., 2009). Another AAA+ ATPase, Cdc48, is an essential protein present in most eukaryotes. It has been reported that
cdc-48.1 and
cdc-48.2, homologs of
cdc48 in C. elegans, are required for appropriate AIR-2 localization prior to cell division in Meiosis I (Sasagawa et al., 2012), implying they may be involved in chromosome partitioning. We therefore decided to test the role of
cdc-48.1 and
cdc-48.2 in SC assembly and disassembly in meiotic prophase. Our results show that in
cdc-48.1 null mutants combined with
cdc-48.2 RNAi, synapsis initiation is delayed, resulting in conglomerations of SC central elements called polycomplexes. While SC does eventually assemble correctly in these mutants, its disassembly is also perturbed, as central elements form large foci near the crossover site on each chromosome in late prophase. Our results thus show that Cdc48 homologs play critical roles in the function of C. elegans meiotic chromosomes. Ferrandiz, N., et al., (2018). Nature Communications, 9(1), 834. Martinez-Perez, E., et al., (2008). Genes & Development, 22(20), 2886-2901. Sasagawa, Y., et al., (2012). Journal of Structural Biology, 179(2), 104-111. Wojtasz, L., et al., (2009). PLoS Genetics, 5(10),
e1000702.