Dosage compensation is the mechanism by which organisms correct the sex chromosome imbalance between sexes (e.g. females having two X chromosomes compared to one X in males). In C. elegans, dosage compensation is achieved by the downregulation by half of both X chromosomes in hermaphrodites (Albritton and Ercan, 2018). This downregulation is accomplished by the Dosage Compensation Complex (DCC), which is comprised of a condensin IDC subcomplex interacting with other accessory proteins. Condensin IDC has a similar structure to canonical condensins (condensin I and condensin II), which function to compact chromosomes during mitosis and meiosis (Csankovszki et al., 2009). The DPY-27 subunit is unique to condensin IDC, MIX-1 is present in all three condensins, while the proteins CAPG-1, DPY-26, and DPY-28 are found both in condensin I and condensin IDC (Figure 1A).DCC mutants show maternal effect lethality, since all subunits of condensin IDC and several of the accessory proteins are maternally contributed to oocytes (Plenefisch et al., 1989; Csankovszki et al., 2009). Homozygous DCC mutants derived from heterozygous mothers survive to adulthood due to the maternally provided RNA and/or protein. These mutants are referred to as maternal positive, zygotic negative (M+Z-). M+Z- hermaphrodites are unable to produce a functional gene product; therefore, their progeny have no maternal or zygotic contribution of these proteins (M-Z-). As a consequence, very few M-Z- hermaphrodites survive past the L1 stage; however, males do not require the DCC to survive. It is possible, then, to recover M-Z- male progeny from self-fertilizing hermaphrodites in these conditions.A previous study (Csankovszki et al. 2009) showed that M+Z-
capg-1 null mutants (
tm1514) are sterile and have severe developmental defects. This phenotype is different from and more severe than what was previously seen for genes encoding other condensin IDC members (Plenefisch et al., 1989). It raised the possibility that the sterility and more severe developmental phenotypes of
capg-1(
tm1514) is the result of another role of CAPG-1 outside of condensin I and IDC function. We acquired another
capg-1 allele (
tm5770) from the Japanese National Bioresource Project. This allele deletes a smaller portion of the coding sequence than
capg-1(
tm1514) but is also predicted to be null due to the resulting frameshift mutation. Also of interest, the
capg-1(
tm5770) allele removes only the terminal nucleotide from a short piRNA gene deleted entirely in
capg-1(
tm1514) (Figure 1B). If the absence of the CAPG-1 protein function was responsible for the sterility phenotype observed in
capg-1(
tm1514), the M+Z- hermaphrodites from the
capg-1(
tm5770) strain should also be sterile.We first confirmed via fluorescence microscopy that the DCC is not recruited to the X chromosome in the
capg-1(
tm1514) adult hermaphrodites, consistent with previously published results (Csankovszki et al., 2009). For additional control, we used a mutation in another condensin IDC member,
dpy-28(
tm3535), which has similar defects (Hernandez et al., 2018). Fluorescent antibodies specific to CAPG-1 and another condensin IDC subunit, DPY-27, were used to visualize localization of the DCC to the X chromosome compared to wild type (N2) (Figure 1C). N2 hermaphrodites have overlapping signals of CAPG-1 and DPY-27 on both X chromosomes. The X localization of these two condensin IDC proteins is also absent in
capg-1(
tm5770). This indicates that the
capg-1(
tm5770) mutation also disrupts DCC localization to the X to a similar degree as
capg-1(
tm1514) or
dpy-28(
tm3535).