Living birth following preimplantation genetic testing for monogenic disorders to prevent low-level germline mosaicism related Nicolaides–Baraitser syndrome
Objective: Paternal sperm mosaicism has few consequences for fathers for mutations being restricted to sperm. However, it could potentially underlie severe sporadic disease in their offspring. Here, we present a live birth of a female infant from a father with low-level sperm DNA mosaicism achieved...
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| Published in | Frontiers in genetics Vol. 13; p. 989041 |
|---|---|
| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Frontiers Media S.A
09.09.2022
|
| Subjects | |
| Online Access | Get full text |
| ISSN | 1664-8021 1664-8021 |
| DOI | 10.3389/fgene.2022.989041 |
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| Abstract | Objective:
Paternal sperm mosaicism has few consequences for fathers for mutations being restricted to sperm. However, it could potentially underlie severe sporadic disease in their offspring. Here, we present a live birth of a female infant from a father with low-level sperm DNA mosaicism achieved
via
preimplantation genetic testing for monogenic disorders (PGT-M).
Methods:
A couple with the father carrying sperm DNA mosaicism received standard
in vitro
fertilization treatment, with intracytoplasmic sperm injection, embryo biopsy, polymerase chain reaction, and DNA analysis. Only one unaffected embryo was transferred to the uterine cavity. Amniocentesis was performed at the 16th week of gestation by copy-number variation-sequencing, karyotyping, and Sanger sequencing.
Results:
Eight surviving embryos were biopsied during the blastocyst stage. Karyomapping and Sanger sequencing were applied to detect the euploidy and paternal mutation. After performing PGT-M, followed by successful pregnancy, the prenatal genetic diagnoses revealed that the fetus was unaffected, and one healthy girl was born.
Conclusion:
This is the first reported live birth with unaffected children achieved
via
PGT for a low-level germline mosaicism father. It not only opens the possibility of preventing the recurrent monogenic disease of children among gonadal mosaicism families but also alerts clinicians to consider gonadal mosaicism as the source of DMNs. |
|---|---|
| AbstractList | Objective: Paternal sperm mosaicism has few consequences for fathers for mutations being restricted to sperm. However, it could potentially underlie severe sporadic disease in their offspring. Here, we present a live birth of a female infant from a father with low-level sperm DNA mosaicism achieved via preimplantation genetic testing for monogenic disorders (PGT-M).Methods: A couple with the father carrying sperm DNA mosaicism received standard in vitro fertilization treatment, with intracytoplasmic sperm injection, embryo biopsy, polymerase chain reaction, and DNA analysis. Only one unaffected embryo was transferred to the uterine cavity. Amniocentesis was performed at the 16th week of gestation by copy-number variation-sequencing, karyotyping, and Sanger sequencing.Results: Eight surviving embryos were biopsied during the blastocyst stage. Karyomapping and Sanger sequencing were applied to detect the euploidy and paternal mutation. After performing PGT-M, followed by successful pregnancy, the prenatal genetic diagnoses revealed that the fetus was unaffected, and one healthy girl was born.Conclusion: This is the first reported live birth with unaffected children achieved via PGT for a low-level germline mosaicism father. It not only opens the possibility of preventing the recurrent monogenic disease of children among gonadal mosaicism families but also alerts clinicians to consider gonadal mosaicism as the source of DMNs. Objective: Paternal sperm mosaicism has few consequences for fathers for mutations being restricted to sperm. However, it could potentially underlie severe sporadic disease in their offspring. Here, we present a live birth of a female infant from a father with low-level sperm DNA mosaicism achieved via preimplantation genetic testing for monogenic disorders (PGT-M). Methods: A couple with the father carrying sperm DNA mosaicism received standard in vitro fertilization treatment, with intracytoplasmic sperm injection, embryo biopsy, polymerase chain reaction, and DNA analysis. Only one unaffected embryo was transferred to the uterine cavity. Amniocentesis was performed at the 16th week of gestation by copy-number variation-sequencing, karyotyping, and Sanger sequencing. Results: Eight surviving embryos were biopsied during the blastocyst stage. Karyomapping and Sanger sequencing were applied to detect the euploidy and paternal mutation. After performing PGT-M, followed by successful pregnancy, the prenatal genetic diagnoses revealed that the fetus was unaffected, and one healthy girl was born. Conclusion: This is the first reported live birth with unaffected children achieved via PGT for a low-level germline mosaicism father. It not only opens the possibility of preventing the recurrent monogenic disease of children among gonadal mosaicism families but also alerts clinicians to consider gonadal mosaicism as the source of DMNs. Objective: Paternal sperm mosaicism has few consequences for fathers for mutations being restricted to sperm. However, it could potentially underlie severe sporadic disease in their offspring. Here, we present a live birth of a female infant from a father with low-level sperm DNA mosaicism achieved via preimplantation genetic testing for monogenic disorders (PGT-M). Methods: A couple with the father carrying sperm DNA mosaicism received standard in vitro fertilization treatment, with intracytoplasmic sperm injection, embryo biopsy, polymerase chain reaction, and DNA analysis. Only one unaffected embryo was transferred to the uterine cavity. Amniocentesis was performed at the 16th week of gestation by copy-number variation-sequencing, karyotyping, and Sanger sequencing. Results: Eight surviving embryos were biopsied during the blastocyst stage. Karyomapping and Sanger sequencing were applied to detect the euploidy and paternal mutation. After performing PGT-M, followed by successful pregnancy, the prenatal genetic diagnoses revealed that the fetus was unaffected, and one healthy girl was born. Conclusion: This is the first reported live birth with unaffected children achieved via PGT for a low-level germline mosaicism father. It not only opens the possibility of preventing the recurrent monogenic disease of children among gonadal mosaicism families but also alerts clinicians to consider gonadal mosaicism as the source of DMNs.Objective: Paternal sperm mosaicism has few consequences for fathers for mutations being restricted to sperm. However, it could potentially underlie severe sporadic disease in their offspring. Here, we present a live birth of a female infant from a father with low-level sperm DNA mosaicism achieved via preimplantation genetic testing for monogenic disorders (PGT-M). Methods: A couple with the father carrying sperm DNA mosaicism received standard in vitro fertilization treatment, with intracytoplasmic sperm injection, embryo biopsy, polymerase chain reaction, and DNA analysis. Only one unaffected embryo was transferred to the uterine cavity. Amniocentesis was performed at the 16th week of gestation by copy-number variation-sequencing, karyotyping, and Sanger sequencing. Results: Eight surviving embryos were biopsied during the blastocyst stage. Karyomapping and Sanger sequencing were applied to detect the euploidy and paternal mutation. After performing PGT-M, followed by successful pregnancy, the prenatal genetic diagnoses revealed that the fetus was unaffected, and one healthy girl was born. Conclusion: This is the first reported live birth with unaffected children achieved via PGT for a low-level germline mosaicism father. It not only opens the possibility of preventing the recurrent monogenic disease of children among gonadal mosaicism families but also alerts clinicians to consider gonadal mosaicism as the source of DMNs. |
| Author | Xu, Chenming Jin, Li Huang, Hefeng Li, Jie Pan, Jiexue Chen, Songchang |
| AuthorAffiliation | 1 Obstetrics and Gynecology Hospital , Institute of Reproduction and Development , Fudan University , Shanghai , China 4 Research Units of Embryo Original Diseases , Chinese Academy of Medical Sciences , Shanghai , China 2 Shanghai Ji Ai Genetics and IVF Institute , Obstetrics and Gynecology Hospital , Fudan University , Shanghai , China 3 Shanghai Key Laboratory of Embryo Original Diseases , Shanghai , China |
| AuthorAffiliation_xml | – name: 1 Obstetrics and Gynecology Hospital , Institute of Reproduction and Development , Fudan University , Shanghai , China – name: 2 Shanghai Ji Ai Genetics and IVF Institute , Obstetrics and Gynecology Hospital , Fudan University , Shanghai , China – name: 4 Research Units of Embryo Original Diseases , Chinese Academy of Medical Sciences , Shanghai , China – name: 3 Shanghai Key Laboratory of Embryo Original Diseases , Shanghai , China |
| Author_xml | – sequence: 1 givenname: Jiexue surname: Pan fullname: Pan, Jiexue – sequence: 2 givenname: Jie surname: Li fullname: Li, Jie – sequence: 3 givenname: Songchang surname: Chen fullname: Chen, Songchang – sequence: 4 givenname: Chenming surname: Xu fullname: Xu, Chenming – sequence: 5 givenname: Hefeng surname: Huang fullname: Huang, Hefeng – sequence: 6 givenname: Li surname: Jin fullname: Jin, Li |
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| Cites_doi | 10.1016/j.rbmo.2011.01.005 10.1038/s41598-017-15814-7 10.1038/344768a0 10.1038/s41588-018-0259-9 10.3389/fped.2021.691761 10.1002/mgg3.2009 10.1038/s41586-020-2347-0 10.7554/eLife.78459 10.1038/nrg3424 10.1530/EJE-19-0472 10.1016/j.tig.2021.05.007 10.1038/ng.3469 10.3389/fgene.2019.01001 10.1016/j.ajhg.2019.04.011 10.1002/mgg3.1763 10.1002/ajmg.c.31409 10.1186/s12920-021-01024-8 10.3389/fgene.2021.633003 10.1093/hmg/4.2.189 10.1186/s13059-016-1110-1 10.1038/s41591-019-0711-0 |
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| Copyright | Copyright © 2022 Pan, Li, Chen, Xu, Huang and Jin. Copyright © 2022 Pan, Li, Chen, Xu, Huang and Jin. 2022 Pan, Li, Chen, Xu, Huang and Jin |
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| Notes | ObjectType-Case Study-2 SourceType-Scholarly Journals-1 ObjectType-Feature-4 content type line 23 ObjectType-Report-1 ObjectType-Article-3 Edited by: Sijia Lu, Yikon Genomics, China Ge Lin, Central South University, China These authors have contributed equally to this work Reviewed by: Fan Jin, Zhejiang University, China This article was submitted to Genetics of Common and Rare Diseases, a section of the journal Frontiers in Genetics |
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Paternal sperm mosaicism has few consequences for fathers for mutations being restricted to sperm. However, it could potentially underlie severe... Objective: Paternal sperm mosaicism has few consequences for fathers for mutations being restricted to sperm. However, it could potentially underlie severe... |
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| SubjectTerms | Genetics Nicolaides–Baraitser syndrome prenatal genetic testing for monogenic disorders recurrent monogenic disease SMARCA2 sperm mosaicism |
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| Title | Living birth following preimplantation genetic testing for monogenic disorders to prevent low-level germline mosaicism related Nicolaides–Baraitser syndrome |
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