Lethal Skeletal Mutants
Lethal Skeletal Mutants - Related Videos
08:39
Shifting Zebrafish Lethal Skeletal Mutant Penetrance by Progeny Testing
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Cited by 8 •
2017
The goal of this protocol is to alter the penetrance of lethal skeletal mutant phenotypes in zebrafish by selective breeding. Lethal mutants cannot be grown to adulthood and bred themselves, therefore this protocol describes a method for tracking and selecting penetrance through multiple generations by progeny testing.
10:51
High-Throughput Robotically Assisted Isolation of Temperature-sensitive Lethal Mutants in Chlamydomonas reinhardtii
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Cited by 8 •
2016
Temperature-sensitive (ts) lethal mutants are valuable tools to identify and analyze essential functions. Here we describe methods to generate and classify ts lethal mutants in high throughput.
14:36
Adult and Embryonic Skeletal Muscle Microexplant Culture and Isolation of Skeletal Muscle Stem Cells
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Cited by 6 •
2010
The micro-dissected explants technique is a robust and reliable method for isolating proliferative skeletal muscle cells from juvenile, adult or embryonic muscles as a source of skeletal muscle stem cells. Uniquely, these cells have been clonally derived to produce skeletal muscle stem cell lines used for in vivo transplantation.
02:41
Lethal Alleles
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2021
Agouti: A Lethal Allele Lucien Cuénot discovered lethal alleles in 1905 while studying the inheritance of coat color in mice. The agouti gene is responsible for the color of the coat in mice. This gene codes for an agouti-signaling protein, which is responsible for melanin distribution in mammals. The wild-type allele gives rise to gray-brown coat color in mice, while the mutant allele gives rise to yellow coat color. In addition to coat color, the agouti gene is associated with the yellow...
09:09
Lethality Bioassay Using Artemia salina L.
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Cited by 20 •
2022
This work aims to evaluate and review the Artemia salina lethality bioassay procedure, also identified as brine shrimp lethality assay. This simple and cheap method gives information about the general toxicity (considered as a preliminary toxicity evaluation) of samples, namely, natural products.
FAQs
A mutation may interrupt signaling pathways, transcriptional programs, tissue patterning, or the differentiation of cartilage and bone. These disruptions can impair skeletal growth, mineralization, or morphogenesis, while also affecting coordinated development with other organs. The resulting phenotype therefore reflects both a direct skeletal defect and broader developmental consequences.
Signaling pathways coordinate developmental instructions between cells and tissues, whereas transcriptional programs control how those instructions alter gene activity. Disrupting either level can change the timing or pattern of skeletal formation. Studying the resulting embryos helps researchers connect altered molecular regulation with specific defects in cartilage, bone, growth, or overall morphogenesis.
Mutant analysis links a defined genetic change to observable alterations in skeletal structure or function. Comparing the mutation with defects in growth, mineralization, differentiation, or tissue patterning helps identify which biological processes depend on the affected gene. This genotype-to-phenotype relationship provides evidence for gene functions that may not be apparent from sequence information alone.
Researchers analyze mutant embryos and tissues for abnormalities in skeletal growth, mineralization, morphogenesis, and the differentiation of cartilage or bone. Observations are interpreted alongside the mutant genotype to determine which developmental processes are disrupted. Because some mutants die embryonically or soon after birth, examining the appropriate developmental stage is essential for capturing their phenotype.
These mutants can reveal whether a gene is required for cartilage differentiation, bone differentiation, mineralization, or the coordinated shaping of skeletal structures. Distinct abnormalities provide clues about where a developmental process has failed. Such comparisons help separate roles in tissue specification, skeletal growth, structural formation, and later functional maturation.
They provide experimental models for investigating gene function, developmental mechanisms, and congenital skeletal disorders. By studying embryos and tissues with defined mutations, researchers can identify molecular and cellular events that underlie abnormal skeletal development. The findings may also inform potential therapeutic strategies by clarifying which processes or pathways are associated with disease-related phenotypes.