Therefore, it has been considered that low temperature adaptation may involve mechanisms opposite to those of high temperature adaptation, based on some single protein comparisons (Nakashima et al. 2003; Siglioccolo et al. 2010); for example, more flexible proteins with reduced hydrophobic cores, less charged surfaces, and more glycine residues (Feller 2010; Reed et al. 2013).
The mechanism underlying this phenomenon is unclear, but may involve neural or humoral adaptations.
These adaptations may involve physiological (e.g., water use efficiency), phenological (e.g., flowering time), or morphological characteristics (e.g., number of leaves).
Co-evolution between the information users and sources in different populations may involve a variable series of adaptations and counter-adaptations leading to ever more intricate patterns of social information use.
Traditionally, adaptation was considered to reflect neural or synaptic "fatigue"; more recent work indicates that adaptation may involve more complex processes (59– 61).
The mechanisms of cancer cell redox adaptation may involve multiple pathways to activate redox-sensitive transcription factors such as NF-κB or Nrf-2 [16], [16] which can, among others, lead to the increased expression of anti-oxidant molecules such as SOD, catalase, thioredoxin and the GSH anti-oxidant system [17].
Tolerance to salinity is commonly reflected in plant growth, which varies as the response progresses, and each phase of the adaptation may involve different signaling pathways [ 7].
Adaptation to anthropogenic climate change in this species may therefore proceed largely from standing variants, and our results suggest this adaptation may involve fewer loci than is often assumed by the infinitesimal model underlying classical quantitative genetics (Barrett and Schluter 2008).
Because adaptation may involve the structure of virulence factors (by antigenic variation) and their regulation, we extended our studies on the evolution of B. pertussis by investigating polymorphism in the promoter of Ptx (ptxP), a major virulence factor and component of all pertussis vaccines (1 ).
The mechanisms underlying these associations may involve fetal cardiovascular and metabolic adaptations in response to increased transport of specific fatty acids to the placenta and fetus [ 16].
