Combined central and peripheral demyelination (CCPD) encompasses a wide array of disorders ranging from myeloradiculoneuritis and encephalomyeloradiculoneuritis, which often occur after infection or vaccination, to co-occurrence of multiple sclerosis (MS) and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP).1,2 Acknowledgment: The authors thank Dr. Isabel Illa (Hospital de la Santa Creu I Sant Pau de Barcelona, Universitat Autònoma de Barcelona, Spain) for providing the control NF155-positive CIDP serum; Dr. Fabio Blandini (C. Mondino National Neurological Institute, IRCCS, Pavia, Italy) for providing the rat sciatic nerves; and Dr. Emilio Ciusani (IRCCS Foundation, C. Besta Neurological Institute, Milan, Italy) for contributing with CCPD sera collection.

In B. subtilis swarming and robust swimming motility require the positive trigger of SwrA on fla/che operon expression. Despite having an essential and specific activity, how SwrA executes this task has remained elusive thus far. We demonstrate here that SwrA acts at the main σ^A-dependent fla/che promoter P_A(fla/che) through DegU. Electrophoretic mobility shift assays (EMSA) reveal that SwrA forms a complex with the phosphorylated form of DegU (DegU~P) at P_A(fla/che) while it is unable to do so with either unphosphorylated DegU or the DegU32(Hy) mutant protein. Motility assays show that a highly phosphorylated DegU is not detrimental for flagellar motility provided that SwrA is present; however, DegU~P represses P_A(fla/che) in the absence of SwrA. Overall, our data support a model in which DegU~P is a dual regulator, acting either as a repressor when alone or as a positive regulator of P_A(fla/che) when combined with SwrA. Finally, we demonstrate that the σ^D-dependent P_D3(fla/che) promoter plays an important role in motility, representing a contingent feedback loop necessary to maintain basal motility when swrA is switched to the non-functional swrA^- status.