Sequence-specific transcription factors (TFs) bind to a small fraction of their sequence motifs in the genome. TF cooperativity and chromatin structure influence TF specificity. Here, we studied the factors that lead to X-chromosome specific targeting of a specialized condensin complex that constitutes the core of the C. elegans dosage compensation complex (DCC). Based on the ChIP-seq analysis of DCC recruiters, genomic distribution of the DCC recruitment DNA sequence motif, histone modifications and histone occupancy, we found that the DCC recruiter SDC-2 is required to open chromatin to allow DCC binding to clusters of motifs on the X chromosome. Thus, DNA sequence motif clustering and chromatin explain part of the specificity of DCC binding. However, motif and chromatin do not explain why some DCC recruitment sites with fewer motifs on the X are bound, and why some strong motif clusters on autosomes are not bound. To address this, we inserted different recruitment sites on the autosomes and tested their ability to recruit. Our results suggest a model in which long-distance cooperation between recruitment sites increase X-specificity of DCC recruitment. Extending this observation to other systems would imply a function for three-dimensional conformation of chromosomes in regulating specificity of protein targeting.