Bernhardt 2015 Abstract MiPschool Greenville 2015: Difference between revisions
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{{Abstract | {{Abstract | ||
|title=Regulation of Ca<sup>2+</sup> entry during oocyte maturation and following fertilization | |||
|authors=Bernhardt ML, Padilla-Banks E, Zhang Y, McDonough CE, Miao YL, Williams CJ | |||
|year=2015 | |year=2015 | ||
|event=MiPschool Greenville 2015 | |event=MiPschool Greenville 2015 | ||
|abstract=Activation of mammalian embryonic development relies on a series of fertilization-induced increases in intracellular Ca<sup>2+</sup>. Full egg activation also requires influx of extracellular Ca<sup>2+</sup>, but the channel or channels mediating this influx remain unknown. In these studies we examined whether T-type Ca<sup>2+</sup> channels, including CACNA1H subunit-containing CaV3.2 channels, mediate Ca<sup>2+</sup> entry after fertilization. We found that female mice lacking CACNA1H have reduced litter size. Careful analysis of Ca<sup>2+</sup> oscillation patterns following ''in vitro'' fertilization (IVF) of ''Cacna1h<sup>-/-</sup>'' eggs revealed shortening of the first Ca<sup>2+</sup> transient length and reduction in Ca<sup>2+</sup> oscillation persistence. Both total and endoplasmic reticulum (ER) Ca<sup>2+</sup> stores in ''Cacna1h<sup>-/-</sup>'' eggs were reduced, showing an impairment of Ca<sup>2+</sup> accumulation during oocyte maturation in ''Cacna1h<sup>-/-</sup>'' eggs. Pharmacological inhibition of T-type channels during ''in vitro'' maturation also reduced Ca<sup>2+</sup> store accumulation, indicating that T-type channels are responsible for mediating Ca<sup>2+</sup> entry and ER store accumulation during meiotic maturation. T-type channel inhibition also reduced oscillation persistence, frequency, and duration following IVF in wild-type eggs. Together, these data support previously unrecognized roles for T-type Ca<sup>2+</sup> channels in mediating the maturation-associated increase in ER Ca<sup>2+</sup> stores and allowing Ca<sup>2+</sup> influx required for the activation of embryo development. In future studies, we plan to investigate how fluxes in oocyte Ca<sup>2+</sup> and Zn<sup>2+</sup> influence mitochondrial function, which is a critical determinant of oocyte and embryo quality. Developing better understanding of the interplay between these pathways may translate into clinical application to improve assisted reproductive technologies. | |||
}} | |||
{{Labeling | |||
|area=Developmental biology | |||
|organism=Mouse | |||
}} | }} | ||
== Affiliations == | == Affiliations == | ||
Reproductive Developm Biol Lab, Nat Inst Health, Nat Inst Health, Research Triangle Park, NC, USA | |||
Revision as of 14:48, 1 July 2015
Regulation of Ca2+ entry during oocyte maturation and following fertilization |
Link:
Bernhardt ML, Padilla-Banks E, Zhang Y, McDonough CE, Miao YL, Williams CJ (2015)
Event: MiPschool Greenville 2015
Activation of mammalian embryonic development relies on a series of fertilization-induced increases in intracellular Ca2+. Full egg activation also requires influx of extracellular Ca2+, but the channel or channels mediating this influx remain unknown. In these studies we examined whether T-type Ca2+ channels, including CACNA1H subunit-containing CaV3.2 channels, mediate Ca2+ entry after fertilization. We found that female mice lacking CACNA1H have reduced litter size. Careful analysis of Ca2+ oscillation patterns following in vitro fertilization (IVF) of Cacna1h-/- eggs revealed shortening of the first Ca2+ transient length and reduction in Ca2+ oscillation persistence. Both total and endoplasmic reticulum (ER) Ca2+ stores in Cacna1h-/- eggs were reduced, showing an impairment of Ca2+ accumulation during oocyte maturation in Cacna1h-/- eggs. Pharmacological inhibition of T-type channels during in vitro maturation also reduced Ca2+ store accumulation, indicating that T-type channels are responsible for mediating Ca2+ entry and ER store accumulation during meiotic maturation. T-type channel inhibition also reduced oscillation persistence, frequency, and duration following IVF in wild-type eggs. Together, these data support previously unrecognized roles for T-type Ca2+ channels in mediating the maturation-associated increase in ER Ca2+ stores and allowing Ca2+ influx required for the activation of embryo development. In future studies, we plan to investigate how fluxes in oocyte Ca2+ and Zn2+ influence mitochondrial function, which is a critical determinant of oocyte and embryo quality. Developing better understanding of the interplay between these pathways may translate into clinical application to improve assisted reproductive technologies.
Labels: MiParea: Developmental biology
Organism: Mouse
Affiliations
Reproductive Developm Biol Lab, Nat Inst Health, Nat Inst Health, Research Triangle Park, NC, USA