Maternal Factor Deletion
Maternal Factor Deletion - Related Videos
09:17
Generation of Maternal Mutants Using zpc:cas9 Knock-in Zebrafish
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2025
Here, we describe a protocol for generating maternal mutant that couples a stable zpc:cas9 knock-in line with Tol2-mediated delivery of sgRNA expression cassettes.
11:24
Rapid Deletion Production in Fungi via Agrobacterium Mediated Transformation of OSCAR Deletion Constructs
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Cited by 8 •
2017
Gene deletion mutants generated through homologous recombination are the gold standard for gene function studies. The OSCAR (One Step Construction of Agrobacterium-Recombination-ready-plasmids) method for rapid generation of deletion constructs is described. Agrobacterium mediated fungal transformation follows. Finally, a PCR based confirmation method of gene deletions in fungal transformants is presented.
07:51
Isolation of Leukocytes from the Murine Tissues at the Maternal-Fetal Interface
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Cited by 44 •
2015
Described herein is a protocol to isolate and analyze the infiltrating leukocytes of tissues at the maternal-fetal interface (uterus, decidua, and placenta) of mice. This protocol maintains the integrity of most cell surface markers and yields enough viable cells for downstream applications including flow cytometry analysis.
06:55
Assessment of Maternal Vascular Remodeling During Pregnancy in the Mouse Uterus
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Cited by 27 •
2015
This protocol describes a technique to assess changes in the maternal vasculature during pregnancy in mice. Using stereological methods, remodeling of the decidual spiral arteries is assessed quantitatively and the results confirmed qualitatively using immunohistochemistry.
14:07
Genome-wide Gene Deletions in Streptococcus sanguinis by High Throughput PCR
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Cited by 9 •
2012
An efficient genome-wide single gene mutation method has been established using Streptococcus sanguinis as a model organism. This method has achieved via high throughput recombinant PCRs and transformations.
FAQs
Maternal messenger RNAs and proteins are deposited in the oocyte before fertilization, so they can direct early cellular events while embryonic transcription has not yet begun. Their presence allows developmental programs to proceed during this transcriptionally dependent interval. Removing a specific product therefore helps reveal which early processes require inherited maternal instructions.
Comparing maternal mutants with zygotic and maternal-zygotic mutants separates effects caused by oocyte-inherited products from those produced after embryonic transcription begins. A maternal phenotype points to an early inherited requirement, whereas differences between single and combined mutant conditions can indicate whether maternal and later embryonic contributions overlap or act at distinct developmental stages.
Oocyte-specific removal focuses the experiment on the maternal contribution rather than eliminating the gene product indiscriminately throughout the organism. This timing is important because the same factor may have functions both before and after zygotic genome activation. Depletion in the oocyte therefore helps connect an observed early phenotype to the inherited product itself.
The approach can reveal maternal requirements for cleavage, cell fate specification, axis formation, and zygotic genome activation. These processes represent different aspects of early development, from initial embryonic divisions to the establishment of identities and body organization. Phenotypic analysis across them helps identify the developmental stage at which the missing maternal product is most influential.
Supported approaches include germline-specific genetic strategies, conditional recombination, and targeted degradation in oocytes. Germline-specific methods focus the manipulation on the lineage that produces oocytes, conditional recombination provides controlled genetic removal, and targeted degradation directly reduces the selected product. The strategy chosen determines how specifically the maternal contribution can be examined.
A useful comparison includes maternal, zygotic, and maternal-zygotic mutant conditions. Examining these groups together shows whether a phenotype follows loss of the inherited oocyte product, loss of the embryonic contribution, or both. This comparison strengthens interpretation by linking developmental outcomes to the timing and source of gene-product activity.
Researchers can use this approach to ask how inherited gene products control development before embryonic transcription begins and how those effects relate to later embryonic functions. In particular, it connects maternal contributions with cleavage, cell fate specification, axis formation, and zygotic genome activation, providing a framework for separating early inherited control from post-transcriptional embryonic control.