Brassinosteroids (BR) have centrally important functions in plant growth by promoting cell proliferation and cell expansion through phosphorylation-mediated regulatory cascades that are initiated by perception of BR by receptor-like kinases of the BRI1 family. These BR-mediated growth responses have been explained by transcriptional controls mediated by phosphorylation of BES1/BZR1 transcription factors. Here we link BRI1-mediated phosphorylation to another growth regulatory network that directly mediates protein stability. BRI1 and its co-receptor BAK1 phosphorylate and inhibit the activities of the growth repressor DA1 by promoting the formation of high molecular weight complexes. Phospho-mimic forms of DA1 are less active while phospho-dead mutants have increased growth-repressive activity, while their regulatory monoubiquitylation is unaffected. BR inhibition of DA1 activity maintains higher levels of DA1 substrates such as UBP15 that sustain the potential for cell proliferation during leaf growth. Reduced BR levels lead to activation of DA1 peptidase activity and a transition from cell proliferation to cell growth and differentiation. This dual monoubiquitylation-phosphorylation regulation supports the key role of BR levels in maintaining the proliferative potential of cells during organ growth.

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The relationship between carotid occlusion response and mean arterial pressure, after small successive hemorrhages, was investigated in the cat anesthetized with α-chloralose. Carotid occlusion response decreased as arterial pressure fell to a level of about 130 mm Hg, but below this level, carotid occlusion response increased. This increase was found to be due to carotid chemoreceptor activity, as it disappeared when the animal breathed oxygen immediately prior to and during the occlusion and was absent in animals after carotid chemoreceptor inactivation. This increase was not present in animals anesthetized with sodium pentobarbital. As this increase was also present in the unanesthetized animal, pentobarbital in anesthetic doses must block the effect of carotid chemoreceptor activity, probably by a central action. In 20% of the animals the carotid occlusion response increased after the first few hemorrhages by an amount equal to the fall in arterial pressure. This increase was not due to chemoreceptor activity, but was probably due to a ceiling phenomenon.

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