Animal asymmetry

problems and defects in mucus clearance that are characteristic of primary cilliary dyskinesia, a disorder of motile cilia. Anything related to signaling? This is one of the most exciting aspects of primary cilium biology and BBSome function. In the ear of bbs knockout animals, hair cells frequently fail to align with one another, a characteristic of defective planar cell polarity (PCP). Although cilia are now known to be essential for PCP in vertebrates, no one knows the identity of the relevant signals sensed and transduced by cilia. Do cilia sense a morphogen gradient that instructs polarity within the plane of the epithelium? Or are cilia facilitating planar cell polarization established at cell–cell contacts by relaying a permissive signal? On the obesity front, bbs mutant mice are unable to transduce leptin signals in specialized hypothalamic neurons that control feeding behavior. Since the leptin receptor was found to interact with a BBSome subunit, it has been hypothesized that the leptin receptor may get trafficked to cilia by the BBSome. However, to this date, no one has succeeded in visualizing the leptin receptor in cilia of the relevant neuronal cell types. Nonetheless, the discovery that IFT dysfunction also causes unregulated weight gains in mice makes the ciliary hypothesis of leptin signaling extremely appealing. What remains to be explored? Nearly everything! What are the membrane proteins that require the BBSome for their trafficking? Does the BBSome function only in trafficking to cilia or is it also involved in IFT or trafficking out of cilia? What is the molecular activity of the BBSome? Does it have any enzymatic activity? What is the function of the BBS proteins that do not belong to the BBSome? In particular, does BBS3/Arl6 function in vesicular trafficking? How and where is the BBSome assembled? Do the type II chaperonin-like BBS proteins BBS6, BBS10 and BBS12 play a role in the folding or assembly of BBSome subunits? Where can I find out more? complex of BBS proteins cooperates with the GTPase Rab8 to promote ciliary membrane biogenesis. For decades morphological asymmetries have evoked curiosity and wonder (Figure 1). Although largely studied by natural history connoisseurs, many wonderful stories emerged: for instance, lopsided flatfish that lie on one side of their body and have both eyes on the other; the narwhal's spectacular, sinistrally-coiled and left-sided tusk; Velella velella, the by-the-wind sailor that drifts on the ocean surface and has right-and left-sailing forms; …