Nuclear Dbf2-related (NDR) kinases play a central role in limiting growth in most animals. Signals that promote growth do so in part by suppressing the activation of NDR kinases by STE20/Hippo kinases. Here, we identify another mechanism for downregulating NDR kinase activity. Specifically, we show that activity of the Drosophila NDR kinase Warts in the developing wing depends on its transition from an inactive, “closed” conformation to a potentially active, “open” conformation mediated by Mats, a conserved Mps1-binder (Mob) protein. Further, we show that signaling interactions between the protocadherins Fat and Dachsous, organized by the morphogens Wingless and Decapentaplegic, suppress Warts by acting via the atypical myosin Dachs to inhibit or reverse this transition. The regulation of Warts conformation by Mats, Fat/Dachsous signaling, and Dachs appears independent of Warts phosphorylation by Hippo kinase, establishing a precedent for the control of NDR kinases, and hence growth, by distinct allosteric and phosphorylation mechanisms.

Urinary bilirubin can be determined as the zinc (II)-azobilirubin complex. The method is similar in principle to the technique of Michaëlsson, but presents some advantages. Being of equal sensitivity and of comparable accuracy and reproducibility, the present procedure can be restricted for routine work to measuring the extinction on two solutions only. No accessory correction term is required, which allows accurate determination of low bilirubin concentrations. Selectivity of the method is good.

A series of metal-azobilirubin complexes is described. In all cases the addition of metal ion produced a considerable shift of the azopigment spectrum to longer wave lengths. The coloured reaction products are stable, the blanks very low.