## 1 Introduction  
Active enhancers can undergo bidirectional transcription [1, 2], producing non-coding RNAs known as enhancer RNAs (eRNAs) [1, 3, 4], which typically have short half-lives [5]. However, several studies have reported that some eRNAs play roles in regulating target gene expression [6, 7, 8, 9, 10]. The modes of action of eRNAs include (1) altering the chromatin environment and enhancing chromatin accessibility to allow more access for transcription factors and other regulatory proteins to bind [11]; (2) facilitating enhancer-promoter interactions [9, 12]; (3) recruiting regulators to facilitate transcription, including chromatin-modifying enzymes, cohesin, transcription factors, coactivators, etc. [9, 13, 14, 15, 16, 17, 18, 19, 20]; and (4) facilitating RNAPII pause-release [10, 21]. eRNAs may act in cis to regulate neighboring genes or act in trans, diffusing within the nucleus to regulate genes across the genome [22, 23]. The regulation of erythropoiesis involves numerous non-coding RNAs [24, 25, 26, 27], for example, lncRNA (UCA1) functions as a scaffold to recruit PTBP1 to stabilize ALAS2 mRNA [28]. A loss of UCA1 will inhibit heme synthesis and block erythroid differentiation at the proerytroblast stage [28]. Trans-acting eRNAs were also reported to participate in regulating erythropoiesis [29, 30]. Although many non-coding RNAs have been reported to be involved in erythropoiesis regulation, a comprehensive understanding is still lacking.  
Cohesin and CTCF have both been reported to interact with RNA [9, 23, 31, 32, 33, 34, 35, 36]. Chromatin looping established by cohesin and CTCF is reduced upon RNA depletion, either through RNase treatment or eRNA knockdown [9, 35, 36]. eRNAs have also been reported to recruit the CTCF/cohesin complex to target gene loci, thereby activating their transcription [23]. However, the interaction between CTCF and RNA is controversial. Whilesome studies suggest that RNA binding is essential for CTCF's role in gene expression and chromatin organization [35; 36], [PERSON] et al. argued that RNA binding by CTCF is a technical artifact [37], although this conclusion may stem from data misanalysis [38]. Nevertheless, the detailed mechanism through which the CTCF/cohesin complex may interact with eRNAs and the functions of their interaction on gene expression are not fully understood.  
We analyzed published RNA-seq data from mouse E14.5 fetal liver cells, integrating this with erythroid enhancer information and Promoter Capture HiC data to identify enhancer RNAs with long-range interactions that are expressed in erythroid cells. Among these erythroid-specific, long-range interacting eRNAs, we identified one, _CpoxRNA_, derived from a super enhancer also containing the _Cpox_ gene. The knockdown of _CpoxRNA_ by shRNA results in impaired proliferation and enucleation during terminal erythropoiesis. Additionally, _CpoxRNA_ plays an architectural role in mediating chromatin looping between its genomic locus and TAD boundaries, as these interactions are reduced upon _CpoxRNA_ loss. We found that _CpoxRNA_ interacts with the CTCF/cohesin complex, migrating to other chromatin loci to regulate genes important for erythropoiesis.