Molecular adapter that acts as a bridge between a variety of multiprotein complexes, and which is involved in antifungal innate immunity, development of the muscle and sister chromatid cohesion (PubMed:23363597, PubMed:30036395, PubMed:30563860, PubMed:31767636). Plays a role in antifungal innate immunity by acting as a bridge between components of the NuRD (Nucleosome Remodeling and Deacetylase) and MEC chromatin remodeling complexes (PubMed:30036395). NuRD and MEC complexes bind to the promoters of antimicrobial peptide genes and may recruit other proteins such as ceh-18 to control gene expression in response to fungal infection (PubMed:30036395). During meiotic prophase I, plays a role in the disassembly of synaptonemal complex proteins and in the regulation of chromosome condensation and segregation (PubMed:23363597). Together with nuclear import receptor ima-2, required for the import and load of cohesin complex proteins in meiotic nuclei, possibly by acting as a bridge between ima-2 and cohesins (PubMed:30563860). Required for embryonic development of muscle tissue (PubMed:31767636). Interacts with hda-1, a component of the NuRD complex (PubMed:30036395). Interacts with let-418, a component of the NuRD and MEC complexes (PubMed:30036395). Interacts with the transcription factor ceh-18 (PubMed:30036395). Interacts with ima-2 (PubMed:30563860). Localizes to somatic tissues throughout the body, including muscle cells (PubMed:31767636). Expressed in lateral epithelial seam cells, the hyp7 epidermal syncytium, and multiple head and tail neurons (PubMed:30036395). Expressed from the late embryo stage onwards, with high expression at the late L4 stage of larval development. 16% embryonic lethality, reduced egg laying and a 0.9% increase in the number of male progeny (PubMed:23363597). Delayed progression of meiosis, which most likely results from defective disassembly of synaptonemal complex proteins, and defective chromosome structure, alignment and condensation (PubMed:23363597). RNAi-mediated knockdown results in reduced expression of the nlp-29 antimicrobial peptide following fungal infection by D.coniospora (PubMed:30036395). Worms show reduced body size and muscle function (PubMed:31767636). Worms lacking both akir-1 and ima-2 show reduced gonad size and aberrant diakinesis oocyte formation; defects are caused by impaired meiotic recombination (PubMed:30563860). Belongs to the akirin family.