When is embryonic arrest broken in turtle eggs?

Research output: Contribution to journalArticleResearchpeer-review

7 Citations (Scopus)

Abstract

Turtle embryos enter a state of arrested development in the oviduct, allowing the mother greater flexibility in her reproductive schedule. Development recommences once eggs transition from the hypoxic oviduct to the normoxic nest. Significant mortality can occur if turtle eggs are moved between 12 h and 20 d after oviposition, and this is linked to the recommencement of embryonic development. To better understand the timing of developmental arrest and to determine how movement-induced mortality might be avoided, we determined the latency (i.e., time elapsed since oviposition) to recommencement of development following oviposition by exposing the eggs of green turtles (Chelonia mydas) to hypoxia (oxygen tension <8 mmHg) for 3 d, commencing 30 min to 48 h after oviposition. Embryonic devel-opment—including development of the characteristic opaque white spot on the eggshell—was halted by hypoxic incubation. When the delay before hypoxic incubation was 12 h or less, hatching success did not differ from a control group. If the hypoxic treatment began after 16 h or more in normoxia, then all embryos died. Thus, by returning eggs to a hypoxic environment before they have broken from arrest (i.e., within 12 h of oviposition), it is possible to extend embryonic arrest for at least 3 d, with no apparent detriment to hatching success. Therefore, hypoxic incubation may provide a new approach for avoidance of movement-induced mortality when conservation or research efforts require the relocation of eggs. Our findings also suggest that movement-induced mortality may have constrained the evolution of viviparity in turtles.

Original languageEnglish
Pages (from-to)523-532
Number of pages10
JournalPhysiological and Biochemical Zoology
Volume90
Issue number5
DOIs
Publication statusPublished - 1 Sep 2017

Keywords

  • Arrested development
  • Embryo
  • Oxygen
  • Preovipositional arrest
  • Reproduction
  • Turtle

Cite this

@article{0d3f0fdb9ce74e0182be761989e60716,
title = "When is embryonic arrest broken in turtle eggs?",
abstract = "Turtle embryos enter a state of arrested development in the oviduct, allowing the mother greater flexibility in her reproductive schedule. Development recommences once eggs transition from the hypoxic oviduct to the normoxic nest. Significant mortality can occur if turtle eggs are moved between 12 h and 20 d after oviposition, and this is linked to the recommencement of embryonic development. To better understand the timing of developmental arrest and to determine how movement-induced mortality might be avoided, we determined the latency (i.e., time elapsed since oviposition) to recommencement of development following oviposition by exposing the eggs of green turtles (Chelonia mydas) to hypoxia (oxygen tension <8 mmHg) for 3 d, commencing 30 min to 48 h after oviposition. Embryonic devel-opment—including development of the characteristic opaque white spot on the eggshell—was halted by hypoxic incubation. When the delay before hypoxic incubation was 12 h or less, hatching success did not differ from a control group. If the hypoxic treatment began after 16 h or more in normoxia, then all embryos died. Thus, by returning eggs to a hypoxic environment before they have broken from arrest (i.e., within 12 h of oviposition), it is possible to extend embryonic arrest for at least 3 d, with no apparent detriment to hatching success. Therefore, hypoxic incubation may provide a new approach for avoidance of movement-induced mortality when conservation or research efforts require the relocation of eggs. Our findings also suggest that movement-induced mortality may have constrained the evolution of viviparity in turtles.",
keywords = "Arrested development, Embryo, Oxygen, Preovipositional arrest, Reproduction, Turtle",
author = "Williamson, {Sean A.} and Evans, {Roger G.} and Reina, {Richard D.}",
year = "2017",
month = "9",
day = "1",
doi = "10.1086/692630",
language = "English",
volume = "90",
pages = "523--532",
journal = "Physiological and Biochemical Zoology",
issn = "1522-2152",
publisher = "The University of Chicago Press",
number = "5",

}

When is embryonic arrest broken in turtle eggs? / Williamson, Sean A.; Evans, Roger G.; Reina, Richard D.

In: Physiological and Biochemical Zoology, Vol. 90, No. 5, 01.09.2017, p. 523-532.

Research output: Contribution to journalArticleResearchpeer-review

TY - JOUR

T1 - When is embryonic arrest broken in turtle eggs?

AU - Williamson, Sean A.

AU - Evans, Roger G.

AU - Reina, Richard D.

PY - 2017/9/1

Y1 - 2017/9/1

N2 - Turtle embryos enter a state of arrested development in the oviduct, allowing the mother greater flexibility in her reproductive schedule. Development recommences once eggs transition from the hypoxic oviduct to the normoxic nest. Significant mortality can occur if turtle eggs are moved between 12 h and 20 d after oviposition, and this is linked to the recommencement of embryonic development. To better understand the timing of developmental arrest and to determine how movement-induced mortality might be avoided, we determined the latency (i.e., time elapsed since oviposition) to recommencement of development following oviposition by exposing the eggs of green turtles (Chelonia mydas) to hypoxia (oxygen tension <8 mmHg) for 3 d, commencing 30 min to 48 h after oviposition. Embryonic devel-opment—including development of the characteristic opaque white spot on the eggshell—was halted by hypoxic incubation. When the delay before hypoxic incubation was 12 h or less, hatching success did not differ from a control group. If the hypoxic treatment began after 16 h or more in normoxia, then all embryos died. Thus, by returning eggs to a hypoxic environment before they have broken from arrest (i.e., within 12 h of oviposition), it is possible to extend embryonic arrest for at least 3 d, with no apparent detriment to hatching success. Therefore, hypoxic incubation may provide a new approach for avoidance of movement-induced mortality when conservation or research efforts require the relocation of eggs. Our findings also suggest that movement-induced mortality may have constrained the evolution of viviparity in turtles.

AB - Turtle embryos enter a state of arrested development in the oviduct, allowing the mother greater flexibility in her reproductive schedule. Development recommences once eggs transition from the hypoxic oviduct to the normoxic nest. Significant mortality can occur if turtle eggs are moved between 12 h and 20 d after oviposition, and this is linked to the recommencement of embryonic development. To better understand the timing of developmental arrest and to determine how movement-induced mortality might be avoided, we determined the latency (i.e., time elapsed since oviposition) to recommencement of development following oviposition by exposing the eggs of green turtles (Chelonia mydas) to hypoxia (oxygen tension <8 mmHg) for 3 d, commencing 30 min to 48 h after oviposition. Embryonic devel-opment—including development of the characteristic opaque white spot on the eggshell—was halted by hypoxic incubation. When the delay before hypoxic incubation was 12 h or less, hatching success did not differ from a control group. If the hypoxic treatment began after 16 h or more in normoxia, then all embryos died. Thus, by returning eggs to a hypoxic environment before they have broken from arrest (i.e., within 12 h of oviposition), it is possible to extend embryonic arrest for at least 3 d, with no apparent detriment to hatching success. Therefore, hypoxic incubation may provide a new approach for avoidance of movement-induced mortality when conservation or research efforts require the relocation of eggs. Our findings also suggest that movement-induced mortality may have constrained the evolution of viviparity in turtles.

KW - Arrested development

KW - Embryo

KW - Oxygen

KW - Preovipositional arrest

KW - Reproduction

KW - Turtle

UR - http://www.scopus.com/inward/record.url?scp=85021456671&partnerID=8YFLogxK

U2 - 10.1086/692630

DO - 10.1086/692630

M3 - Article

AN - SCOPUS:85021456671

VL - 90

SP - 523

EP - 532

JO - Physiological and Biochemical Zoology

JF - Physiological and Biochemical Zoology

SN - 1522-2152

IS - 5

ER -