Cilia - the prodigal organelle

So why establish a journal devoted to this once forgotten organelle? The reasons are simple: interest and importance. In 1997-1998 there were a handful of publications citing work on primary cilia with the main focus on olfactory receptors (Figure 1). That year however, saw the publication of Nonaka and Hirokawa's seminal paper on nodal cilia and left-right asymmetry which helped kick-start the field [8]. The year 1998 also produced the classic purification of the intraflagellar transport (IFT) complexes from Cole and Rosenbaum [9], providing the molecular basis for previous discovery from Koszminski and Rosenbaum of the intraflagellar transport process [10]. This led in rapid succession to links between polycystic kidney disease and cilia, starting with the link of C. elegans homolog of the PKD1 and PKD2 polycystins, mutated in human polycystic kidney disease, to sensory cilia [11]; the link of IFT-B components to mutations in left-right asymmetry [12]; and the link between the IFT-B complex, the polycystic kidney disease gene tg737 and ciliary assembly [13]. In 2003, work from Kathryn Anderson's lab made the striking connection between primary cilia and Hedgehog signaling [14], which caught the attention of developmental biologists and helped bring cilia into the mainstream of developmental cell biology. A variety of links between cilia and morphogen pathways have since been published, causing both enthusiasm and controversy. The year 2006 saw a 20-fold increase in publications on the topic with an emphasis on the role of cilia in polycystic kidney disease. Since 2007, a growing number of publications have characterized interacting networks of proteins that form critical parts of the ciliary trafficking and signaling machinery, and linked these networks and complexes to the human genetic disease, providing deeper explanations for human genetic diseases like Bardet-Biedl syndrome, nephronophthisis, Joubert, and Meckel-Gruber syndromes. Publications in 2011 continue