Photosynthetic sucrose drives the lateral root clock in Arabidopsis seedlings.

The development of plant roots is subject to control by light. Here, we show that, similar to monotonous root elongation, the periodic induction of lateral roots (LRs) depends on the activation by light of photomorphogenic and photosynthetic photoreceptors in the shoot in a hierarchical order. The prevailing belief is that the plant hormone auxin serves as a mobile signal transmitter, responsible for interorgan communication, including light-controlled shoot-to-root connections.

The plant hormone auxin beats the time for oscillating light-regulated lateral root induction.

The molecular mechanism underlying the periodic induction of lateral roots, a paradigmatic example of clock-driven organ formation in plant development, is a matter of ongoing, controversial debate. Here, we provide experimental evidence that this clock is frequency modulated by light and that auxin serves as a mediator for translating continuous light signals into discontinuous gene activation signals preceding the initiation of lateral roots in seedlings. Based on this evidence, we propose a molecular model of an ultradian biological clock involving auxin-dependent degradation of an AUX/IAA-type transcription repressor as a flexible, frequency-controlling delay element.

Priming and positioning of lateral roots in Arabidopsis. An approach for an integrating concept.

Branching by de novo formation of lateral roots along the primary root of Arabidopsis seedlings follows a complex longitudinal and transverse pattern. How this pattern is generated is presently under debate. The 'bending hypothesis' proposes that lateral root primordia are initiated by a local accumulation of auxin at the convex side of bends resulting from deflections through obstacles, gravitropic bending, or other means.

Inhibition of Cell Expansion by Rapid ABP1-Mediated Auxin Effect on Microtubules? A Critical Comment.

Critical analysis of a recent article raises questions regarding the inhibition of cell expansion by rapid ABP1-mediated auxin effect on microtubules.

Evidence for altered transport of insulin across the blood-brain barrier in insulin-resistant humans.

Eating behavior, body weight regulation, peripheral glucose metabolism, and cognitive function depend on adequate insulin action in the brain, and recent studies in humans suggested that impaired insulin action in the brain emerges upon fat intake, obesity, and genetic variants. As insulin enters into the brain in a receptor-mediated fashion, we hypothesized that whole-body insulin sensitivity might affect the transport of insulin into the brain and contribute to the aversive effect of insulin resistance in the central nervous system. In this study, we aimed to determine the ratio of insulin in the cerebrospinal fluid and serum to whole-body insulin sensitivity.