Figure 2.

Alternative Hypotheses for Lateral Root Priming Oscillations.

(A) Middleton et al. (2010) showed that the induction of AUX/IAA expression by ARF constitutes a negative feedback capable of generating cell-autonomous oscillations in auxin response (ARF) and auxin concentration levels.

(B) Mellor et al. (2016a) proposed a combination of positive feedback between auxin and LAX3 and a negative feedback between auxin and GH3 to result in cell-autonomous auxin level oscillations.

(C) Left: PIN-driven root tip auxin reflux, with PIN, PIN3, and PIN7 mediated rootward flux in the vascular tissues, apolar outward flux in the columella dependent on PIN3, PIN4, and PIN7, and PIN2-dominated shootward and inward flux in the outer tissues (Blilou et al., 2005). Right: Characteristic cell-level PIN patterns for the different cell types present in the root.

(D) to (F) Flux-based tissue-level mechanisms. Relevant auxin fluxes are indicated by red arrows as described in the key to the right of (F); assumptions underlying the models are indicated with black arrows pointing toward the root, and the resulting spatiotemporal auxin (response) dynamics are indicated with black arrows pointing away from the root.

(D) In the Mironova et al. (2010) model, auxin-dependent regulation of PIN1 is suggested to generate oscillations in auxin levels in the basal meristem. Lower graph: Blue and red lines depict the distinct oscillation phases when auxin (response) levels in the oscillation zone are low or high, respectively. These phases arise as a result of shoot-dependent auxin influx that increases over developmental time (upper blue graph) combined with a dependence of vascular PIN1 levels on auxin levels that follows an optimum curve (middle red graph).

(E) Lucas et al. (2008a) showed that if priming occurs when auxin in the basal meristem exceeds a certain threshold level (thus depleting the pool of auxin in this region) and refilling occurs gradually from the shoot-derived auxin influx and local root tip auxin reflux, oscillations in basal meristem auxin level arise. Developing (but not mature) lateral roots could contribute to this oscillation by consuming auxin flowing from the shoot to the root tip, making lateral root development and priming interdependent.

(F) In the new hypothesis proposed here, we assume an opposite dependence of PINs in the vasculature cells and PIN2 in the outer cells on auxin, cytokinin, and/or PLETHORA. This contrasting regulation is assumed to give rise to out-of-phase oscillations in PIN-mediated rootward auxin fluxes and PIN2-mediated shootward and inward auxin fluxes. Together, this is hypothesized to give rise to transient elevations in auxin levels that travel around the root tip reflux root, causing oscillations in the basal meristem but also possibly modulating the quiescent center auxin maximum.