TheBio‐Logic and machinery of plant morphogenesis

Abstract

Morphogenesis (the development of organic form) requires signal-trafficking and cross-talking across all levels of organization to coordinate the operation of metabolic and genomic networked systems. Many biologists are currently converging on the pictorial conventions of computer scientists to render biological signaling as logic circuits supervising the operation of one or more signal-activated metabolic or gene networks. This approach can redact and simplify complex morphogenetic phenomena and allows for their aggregation into diagrams of larger, more "global" networked systems. This conceptualization is discussed in terms of how logic circuits and signal-activated subsystems work, and it is illustrated for examples of increasingly more complex morphogenetic phenomena, e.g., auxin-mediated cell expansion, entry into the mitotic cell cycle phases, and polar/lateral intercellular auxin transport. For each of these phenomena, a posited circuit/subsystem diagram draws rapid attention to missing components, either in the logic circuit or in the subsystem it supervises. These components must be identified experimentally if each of these basic phenomena is to be fully understood. Importantly, the power of the circuit/subsystem approach to modeling developmental phenomena resides not in its pictorial appeal but in the mathematical tools that are sufficiently strong to reveal and quantify the synergistics of networked systems and thus foster a better understanding of morphogenesis.

A Grammar-Based Model of Barley Including Virtual Breeding, Genetic Control and a Hormonal Metabolic Network

“…Other recent papers have dealt with the modelling of the effect of auxin on various morphogenetic processes (e.g. Rolland-Lagan et al 2003; using L-systems; see also Niklas 2003). We are fully aware that our model is a crude simplification and that for a physiologically reflected view on the process of stem formation, one would have to consider all relevant hormones (auxins, GAs, cytokinins, abscisic acid, ethylene) in one model.…”

Conceptual Change in Biology

“…Although a complex logic circuit can be simplified mathematically, four caveats are evident when biological systems are approached in this way (Niklas 2003): (1) there is no a priori method to determine which among logically equivalent circuits is biologically real, i.e., oversimplification can produce false circuit diagrams; (2) incomplete signaling pathways may appear to 'work' when diagrammed, i.e., missing components are not invariably obvious; (3) parallel logic circuits may obtain invariant output signals that give the appearance that input signals pass through serial switches, i.e., a bifurcating signal transduction pathway is more readily misdiagnosed than a serial pathway; and, (4) nothing in a logic circuit per se indicates when and how long a switch is turned on or off or how long a genomic or metabolic product lasts, i.e., the temporal components of signaling can be lost.…”

Adaptive Aspects of Development: A 30-Year Perspective on the Relevance of Biomechanical and Allometric Analyses

“…This feature governs the working of any networked system and instantiates what I called the biological "incompleteness theorem," i.e., the operation of any biological subsystem cannot be fully diagnosed in isolation of the operations of the other subsystems to which it is networked (Niklas 2003). This theorem, which is an analog to Kurt Gödel's (1931) incompleteness theorems, can be proved mathematically, but it is easily illustrated by a hypothetical example consisting of two nuclear genes (G1, G2), their enhancer-promoters (EP1, EP2), a cell membrane docking Fig.…”

“…This theorem, which is an analog to Kurt Gödel's (1931) incompleteness theorems, can be proved mathematically, but it is easily illustrated by a hypothetical example consisting of two nuclear genes (G1, G2), their enhancer-promoters (EP1, EP2), a cell membrane docking Fig. 2.2 Schematics of a simple, signal-activated subsystem and the "incompleteness theorem" (Adapted from Niklas 2003). (a) A signal-activated (S-A) subsystem with an actuator/suppressor, a subsystem assembly, a feedback element, and a comparator.…”

“…Note that when N ¼ 5, S ¼ 4.29 Â 10 9 . Although a complex logic circuit can be simplified mathematically, four caveats are evident when biological systems are approached in this way (Niklas 2003): (1) there is no a priori method to determine which among logically equivalent circuits is biologically real, i.e., oversimplification can produce false circuit diagrams; (2) incomplete signaling pathways may appear to 'work' when diagrammed, i.e., missing components are not invariably obvious; (3) parallel logic circuits may obtain invariant output signals that give the appearance that input signals pass through serial switches, i.e., a bifurcating signal transduction pathway is more readily misdiagnosed than a serial pathway; and, (4) nothing in a logic circuit per se indicates when and how long a switch is turned on or off or how long a genomic or metabolic product lasts, i.e., the temporal components of signaling can be lost.…”