Abstract
Our developmental environment significantly affects myriad aspects of our biology, including key life history traits, morphology, physiology, and our susceptibility to disease. This environmentally-induced variation in phenotype is known as plasticity. In many cases, plasticity results from alterations in the rate of synthesis of important developmental hormones. However, while developmental processes like organ growth are sensitive to environmental conditions, others like patterning – the process that generates distinct cell identities – remain robust to perturbation. This is particularly surprising given that the same hormones that regulate organ growth also regulate organ patterning. In this review, we revisit the current approaches that address how organs coordinate their growth and pattern, and outline our hypotheses for understanding how organs achieve correct pattern across a range of sizes.
Highlights
Animals vary in their adult body size according to the environmental conditions in which they develop (Angilletta et al, 2004; Hietakangas and Cohen, 2009; Harrison and Haddad, 2011; Nijhout et al, 2014)
This change in size results from modifications of the systemic signals that coordinate the growth of organs and the whole body (Hietakangas and Cohen, 2009). Regardless of their final size, organs retain the same overall pattern: adult humans have the same number of teeth regardless of how large or small their head is. This has long been interpreted as meaning that the developmental patterning programs that establish cell identity are scale-free, independent of those that regulate organ growth (Umulis and Othmer, 2013)
Recent studies suggest that the processes of growth and patterning are far more intertwined than previously thought, and that robustness of final organ pattern is underpinned by surprising plasticity in the rate of pattern formation
Summary
Animals vary in their adult body size according to the environmental conditions in which they develop (Angilletta et al, 2004; Hietakangas and Cohen, 2009; Harrison and Haddad, 2011; Nijhout et al, 2014). If we extrapolate these findings to other animals, we could hypothesize that morphogens confer robustness by reliably inducing cell fates across the range of environmental conditions to which organ growth shows sensitivity. Perhaps the best elucidated example of the systemic control of environmentally-sensitive growth is the effect of nutrition on growth rate via the insulin/insulin-like growth factor signaling (IIS) pathway, a pathway conserved amongst all animals (Hietakangas and Cohen, 2009).
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