Phospholipase C zeta (PLCζ) and the clinical diagnosis of oocyte activation deficiency

Oocyte activation deficiency (OAD) remains the predominant cause of total/low fertilization rate in assisted reproductive technology (ART). Phospholipase C zeta (PLCζ) is the dominant sperm-specific factor responsible for triggering oocyte activation in mammals. OAD has been linked to numerous PLCζ...

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Main Authors: Jones, C, Meng, X, Coward, K
Format: Journal article
Language:English
Published: BioScientifica 2022
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author Jones, C
Meng, X
Coward, K
author_facet Jones, C
Meng, X
Coward, K
author_sort Jones, C
collection OXFORD
description Oocyte activation deficiency (OAD) remains the predominant cause of total/low fertilization rate in assisted reproductive technology (ART). Phospholipase C zeta (PLCζ) is the dominant sperm-specific factor responsible for triggering oocyte activation in mammals. OAD has been linked to numerous PLCζ abnormalities in patients experiencing failed in-vitro fertilization (IVF) or intra-cytoplasmic sperm injection (ICSI) cycles. While significant efforts have enhanced our understanding of the clinical relevance of PLCζ, and the potential effects of genetic variants upon functionality, our ability to apply PLCζ in a diagnostic or therapeutic role remains limited. Artificial oocyte activation (AOA) is the only option for patients experiencing OAD but lacks a reliable diagnostic approach. Immunofluorescence analysis has revealed that the levels and localization patterns of PLCζ within sperm can help us to indirectly diagnose a patient’s ability to induce oocyte activation. Screening of the gene encoding PLCζ protein is also critical if we are to fully determine the extent by which genetic factors might play a role in the aberrant expression and/or localization patterns observed in infertile patients. Collectively, these findings highlight the clinical potential of PLCζ, both as a prognostic indicator of OAD, and eventually as a therapeutic agent. In this review, we focus on our understanding of the association between OAD and PLCζ by discussing the localization and expression of this key protein in human sperm, the potential genetic causes of OAD, and the diagnostic tools that are currently available to us to identify PLCζ deficiency and select patients that would benefit from targeted therapy.
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spelling oxford-uuid:15c5dc5e-350b-4a51-bb94-1e9ff0977a2e2022-07-04T08:56:01ZPhospholipase C zeta (PLCζ) and the clinical diagnosis of oocyte activation deficiencyJournal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:15c5dc5e-350b-4a51-bb94-1e9ff0977a2eEnglishSymplectic ElementsBioScientifica 2022Jones, CMeng, XCoward, KOocyte activation deficiency (OAD) remains the predominant cause of total/low fertilization rate in assisted reproductive technology (ART). Phospholipase C zeta (PLCζ) is the dominant sperm-specific factor responsible for triggering oocyte activation in mammals. OAD has been linked to numerous PLCζ abnormalities in patients experiencing failed in-vitro fertilization (IVF) or intra-cytoplasmic sperm injection (ICSI) cycles. While significant efforts have enhanced our understanding of the clinical relevance of PLCζ, and the potential effects of genetic variants upon functionality, our ability to apply PLCζ in a diagnostic or therapeutic role remains limited. Artificial oocyte activation (AOA) is the only option for patients experiencing OAD but lacks a reliable diagnostic approach. Immunofluorescence analysis has revealed that the levels and localization patterns of PLCζ within sperm can help us to indirectly diagnose a patient’s ability to induce oocyte activation. Screening of the gene encoding PLCζ protein is also critical if we are to fully determine the extent by which genetic factors might play a role in the aberrant expression and/or localization patterns observed in infertile patients. Collectively, these findings highlight the clinical potential of PLCζ, both as a prognostic indicator of OAD, and eventually as a therapeutic agent. In this review, we focus on our understanding of the association between OAD and PLCζ by discussing the localization and expression of this key protein in human sperm, the potential genetic causes of OAD, and the diagnostic tools that are currently available to us to identify PLCζ deficiency and select patients that would benefit from targeted therapy.
spellingShingle Jones, C
Meng, X
Coward, K
Phospholipase C zeta (PLCζ) and the clinical diagnosis of oocyte activation deficiency
title Phospholipase C zeta (PLCζ) and the clinical diagnosis of oocyte activation deficiency
title_full Phospholipase C zeta (PLCζ) and the clinical diagnosis of oocyte activation deficiency
title_fullStr Phospholipase C zeta (PLCζ) and the clinical diagnosis of oocyte activation deficiency
title_full_unstemmed Phospholipase C zeta (PLCζ) and the clinical diagnosis of oocyte activation deficiency
title_short Phospholipase C zeta (PLCζ) and the clinical diagnosis of oocyte activation deficiency
title_sort phospholipase c zeta plcζ and the clinical diagnosis of oocyte activation deficiency
work_keys_str_mv AT jonesc phospholipaseczetaplczandtheclinicaldiagnosisofoocyteactivationdeficiency
AT mengx phospholipaseczetaplczandtheclinicaldiagnosisofoocyteactivationdeficiency
AT cowardk phospholipaseczetaplczandtheclinicaldiagnosisofoocyteactivationdeficiency