Dear Editor,rnCytoplasmic male sterility (CMS) in plants is a matally inherited inability to produce functional pollen.CMS is generally caused by aberrant mitochondrial genes that are often chimeric in structure and frequently co-transcribed with conventional mitochondrial genes (Hanson and Bentolila,2004).In many instances,male sterility can be recovered by nuclear-encoded restorer of fertility (Rf) genes.CMS/Rfsystems serve as an excellent model to study mitochondrial-nuclear coevolution and interaction in plants as well as as a useful genetic tool for breeding to exploit hybrid vigor in crops (Chen and Liu,2014).Polima (pol) CMS,initially reported in China,was the first CMS system used for commercial F1 hybrid seed production in Brassica napus (Witt et al.,1991).The pol CMS system is associated with the presence of a chimeric open reading frame (ORF),orf224,located upstream of atp6,which encodes subunit 6 of mitochondrial ATPase (Singh and Brown,1991;L’Homme and Brown,1993).In the presence of the nuclear restorer gene,Rfp,processing of orf224/atp6 RNA is affected and its transcripts are specifically altered,which suggests that orf224 is the causal gene of pol CMS (Singh and Brown,1991).A previous comparison of RNA-seq data between fertile and sterile young flower buds with pol CMS suggested that energy deficiency caused by orf224/atp6 may inhibit a series of genes that regulate pollen development via nuclear-mitochon-drial interactions (An et al.,2014).However,how orf224/atp6 causes male sterility and how Rfp conditions orf224/atp6 transcription remain unclear.Answering both questions would represent an important step in characterizing Rfp.