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Environmentally‐Induced Phenotypic Plasticity in Embryonic Reptiles
Author(s) -
Crossley Dane Alan,
Elsey Ruth,
Marks Christopher,
Eme John
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1149.13
Subject(s) - phenotypic plasticity , alligator , phenotype , plasticity , embryonic heart , biology , developmental plasticity , embryogenesis , heart development , embryonic stem cell , embryo , incubation , hypoxia (environmental) , medicine , microbiology and biotechnology , endocrinology , genetics , ecology , chemistry , gene , biochemistry , physics , organic chemistry , oxygen , thermodynamics
In response to chronic developmental stress, embryonic reptiles exhibit phenotypic plasticity resulting in morphological and physiological modifications. Utilizing chronic hypoxia, we investigated plasticity of cardiovascular regulatory maturation in two species, American alligator and common snapping turtle. Both exhibit phenotypic plasticity, resulting in increased relative heart mass and depressed heart rate. However, they differ in their capacity to modify the timing of cardioregulatory ability and the strength of each regulatory mechanism during development. We also determined that the cardiovascular system appeared most susceptible to environmentally‐induced phenotypic change during the last third of embryonic development. Relocation of chronically hypoxic‐incubated (10% O 2 ) American alligator embryos to normoxia (H to N) at 70% of incubation returned heart mass to control values measured at 90% of development; the opposite manipulation (N to H) did not increase heart mass. Physiological phenotype was also altered, resulting in a reduced intrinsic heart rate in the N to H shift group compared to the H to N group. These data indicate that the degree of cardiovascular developmental phenotypic plasticity is species dependent and may require exposure during finite (‘critical’) windows of development to produce a given response. NSF CAREER IBN IOS‐0845741 to DAC