Generation of Genome-Edited Chicken Through Targeting of Primordial Germ Cells

Idoko-Akoh, Alewo; McGrew, Michael J.

doi:10.1007/978-1-0716-2990-1_20

Cited by 2 publications

(1 citation statement)

References 13 publications

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“…Genome editing is now possible in the chicken ( Idoko-Akoh and Mcgrew 2023 ). Avian embryos are easily accessible for developmental studies and have been used to observe the distribution of fibrillin-1 during early development ( Burke et al 2000 ).…”

Section: Other Potential Models For Fibrillinopathiesmentioning

confidence: 99%

Genetic models of fibrillinopathies

Summers

2023

Genetics

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The fibrillinopathies represent a group of diseases in which the 10–12 nm extracellular microfibrils are disrupted by genetic variants in one of the genes encoding fibrillin molecules, large glycoproteins of the extracellular matrix. The best-known fibrillinopathy is Marfan syndrome, an autosomal dominant condition affecting the cardiovascular, ocular, skeletal, and other systems, with a prevalence of around 1 in 3,000 across all ethnic groups. It is caused by variants of the FBN1 gene, encoding fibrillin-1, which interacts with elastin to provide strength and elasticity to connective tissues. A number of mouse models have been created in an attempt to replicate the human phenotype, although all have limitations. There are also natural bovine models and engineered models in pig and rabbit. Variants in FBN2 encoding fibrillin-2 cause congenital contractural arachnodactyly and mouse models for this condition have also been produced. In most animals, including birds, reptiles, and amphibians, there is a third fibrillin, fibrillin-3 (FBN3 gene) for which the creation of models has been difficult as the gene is degenerate and nonfunctional in mice and rats. Other eukaryotes such as the nematode C. elegans and zebrafish D. rerio have a gene with some homology to fibrillins and models have been used to discover more about the function of this family of proteins. This review looks at the phenotype, inheritance, and relevance of the various animal models for the different fibrillinopathies.

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Section: Other Potential Models For Fibrillinopathiesmentioning

confidence: 99%

Genetic models of fibrillinopathies

Summers

2023

Genetics

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A male-essential microRNA is key for avian sex chromosome dosage compensation

Fallahshahroudi,

Rodríguez-Montes,

Taemeh

et al. 2024

Preprint

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Birds have a sex chromosome system in which females are heterogametic (ZW) and males are homogametic (ZZ). The differentiation of avian sex chromosomes from ancestral autosomes entailed the loss of most genes from the W chromosome during evolution. However, to what extent mechanisms evolved that counterbalance the consequences of this extensive gene dosage reduction in female birds has remained unclear. Here we report functional in vivo and evolutionary analyses of a Z-chromosome-linked microRNA (miR-2954) with strongly male-biased expression that was previously proposed to play a key role in sex chromosome dosage compensation1. We knocked out miR-2954 in chicken, which resulted in early embryonic lethality of homozygous knockout males, likely due to the highly specific upregulation of dosage-sensitive Z-linked target genes of miR-2954. Our evolutionary gene expression analyses further revealed that these dosage-sensitive target genes have become upregulated on the single Z in female birds during evolution. Altogether, our work unveils a scenario where evolutionary pressures on females following W gene loss led to the evolution of transcriptional upregulation of dosage-sensitive genes on the Z not only in female but also in male birds. The resulting overabundance of transcripts in males resulting from the combined activity of two dosage-sensitive Z gene copies was in turn offset by the emergence of a highly targeted miR-2954-mediated transcript degradation mechanism during avian evolution. Our findings demonstrate that birds have evolved a unique sex chromosome dosage compensation system in which a microRNA has become essential for male survival.

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Generation of Genome-Edited Chicken Through Targeting of Primordial Germ Cells

Cited by 2 publications

References 13 publications

Genetic models of fibrillinopathies

Genetic models of fibrillinopathies

A male-essential microRNA is key for avian sex chromosome dosage compensation

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