Mutations in SMARCAL1, which encodes a DNA annealing helicase with roles in DNA 
replication fork restart, DNA repair, and gene expression modulation, cause 
Schimke immuno-osseous dysplasia (SIOD), an autosomal recessive disease 
characterized by skeletal dysplasia, renal disease, T-cell immunodeficiency, and 
arteriosclerosis. The clinical features of SIOD arise from pathological changes 
in gene expression; however, the underlying mechanism for these gene expression 
alterations remains unclear. We hypothesized that changes of the epigenome alter 
gene expression in SIOD. To test this, we performed a genetic screen for 
interaction between Marcal1, the Drosophila melanogaster ortholog of SMARCAL1, 
and the genes of the trithorax group (trxG) and Polycomb group (PcG), which 
encode epigenetic regulators. SMARCAL1 and Marcal1 genetically interacted with 
trxG and PcG members. A homozygous null mutation of Marcal1 suppressed the 
wing-to-haltere transformation, ectopic Ultrabithorax (Ubx) expression, and 
ectopic Ubx minigene expression caused by PcG deficiency. The suppression of 
ectopic Ubx expression correlated with reduced chromatin accessibility of the 
Ubx promoter. To our knowledge, this is the first in vivo evidence for 
deficiency of a SMARCAL1 ortholog altering the chromatin structure of a gene.