Figure 4. Alleles of Sxl^M8 or the Dosage Compensation Complex (DCC) component male-specific lethal-2 (msl-2) rescues Nab2 phenotypes.

(A) A single copy of the Sxl^M8 allele, which harbors a 110 bp deletion that causes constitutive exon 2-4 splicing, partially suppresses lethality of Nab2^ex3, both zygotically and maternally (calculated as #observed/#expected). (B, C) Sxl^M8 dominantly (i.e., M8/+) suppresses previously defined (B) locomotion (as assessed by negative-geotaxis) and (C) lifespan defects in age-matched Nab2^ex3 females. (D) Percent of control, Nab2^ex3, or msl-2^kmA/+;;Nab2^ex3 (msl-2 is on the X chromosome) that eclose as viable adults (calculated as #observed/#expected). (E, F) msl-2^kmA dominantly (i.e., kmA/+) suppresses previously defined (E) locomotion (as assessed by negative-geotaxis) and (F) lifespan defects in age-matched Nab2^ex3 females. Significance values are indicated (*p<0.05, ****p<0.0001).

Figure 4—figure supplement 1. Additional genetic interactions between Nab2^ex3 msl-2, roX1, and mle.

(A) Adult viability of control females (black bar) with one copy of Nab2^ex3 in a msl-2 deficient background (msl-2²²⁷ truncating allele over Exel7016 deletion), females lacking Nab2 (Nab2^ex3, dark gray bar), or Nab2^ex3 mutant females in msl-2²²⁷/Exel7016 background (light gray bar). (B) Negative geotaxis of age-matched adult female controls (Nab2^pex41), Nab2^ex3 mutants, or Nab2^ex3 mutants carrying single copies of the roX1^e6 or mle⁹ loss-of-function alleles at 5 s, 10 s, and 15 s timepoints. Significance values between indicated groups are indicated at the 30 s timepoint (p-values are indicated; n.s., not significant).