Neural control of body-plan axis in regenerating planaria
Fig 1
A conceptual summary of our model of anterior-posterior axis control in planaria regeneration.
We hypothesize morphogens to be transported on a vector field coincident with neuronal axons (A), with hypothesized transport polarity as shown in (B). We further hypothesize that vector transport of morphogens occurs on aligned microtubule arrays in nerve axons (C, D). A regulatory network (E) integrates molecular-genetic interactions with vector transport in nerves to produce stable, self-assembling morphogen gradients consistent with planarian body-plan in homeostasis (F), and capable of responding to cutting event perturbations to establish new gradients (G). Head and tail regeneration are assumed to be related to concentrations of ERK and β-Cat, respectively (F, G, H). The percentage of regenerated heteromorphoses in a population was estimated from steady-state ERK and β-Cat gradients after cutting (G), where average morphogen concentration at wound edges (G ii, and iii) were used to define the probability of the blastema developing into a head or tail (G, H) using a Markov Chain Model for Regeneration (see text and Fig 3 for details). Head (G, transition ‘i’) and tail (G, transition ‘iv’) regions existing on a fragment prior to cutting were assumed to be terminally differentiated, and to therefore remain as head or tail in the regenerated fragment. In the regulatory network of E, blue lines with circular endpoints represent activating interaction, whereas red lines with flat-line ends represent an inhibitory relationship. Kinesin symbol on Hedgehog node, and dynein symbol on NRF, signify proposed transport of the respective factors. Hh—Hedgehog, Ptc—Patched, Wnt—Wingless/integrated (Wnt1 and Wnt11 combined), β-Cat—β-Catenin, ERK—extracellular-signal regulated kinase, cAMP—cyclic adenosine monophophate, NRF—Notum Regulating Factor.