bioRxiv Science⌕ Search

bioRxiv · 10.1101/2022.11.13.516295

Identification of variation in Fibromelanosis region on chromosome 20 for determining the purity of Indonesian Cemani chicken

Abstract

Ayam Cemani is a local Indonesian chicken with heavy pigmentation in plumage colour, skin, eyes, and inner body organs. This trait with dermal hyperpigmentation is identical to Fibromelanosis (Fm) mutation in a Silkie chicken. The causal mutation of the Fm trait is due to an inverted duplication and junction of two genomic regions involving the Endothelin3 (EDN3) gene on chromosome 20. There are two duplication boundaries; one is specific to the Fm allele, the other is common for both Fm and fm+ allele. Determining birds that are homozygous or heterozygous at this locus is useful for unifying the Fm trait of Cemani populations. This study develops a method for determining the presence or absence of Fm mutation by PCR amplification using the inverted sequences specific to the Fm allele. Further, it develops the restriction fragment length polymorphism (RFLP) method in regions common to the Fm and wild-type fm+ allele. We aim to establish a simple method for detecting homozygous (Fm/Fm) and heterozygous (Fm/fm+) individuals with Fm mutation and to clarify the degree of fixation of the Fm trait in the Ayam Cemani populations and the association between the phenotype and genotype. The result showed that mostly, the phenotype for Cemani with Fm/ fm+ genotype is reddish black in their comb; meanwhile, the Cemani with (Fm/Fm) genotype showed heavy black pigmentation. Our study concluded that using the PCR-RFLP method. We can discriminate between Fm homozygous and heterozygous birds in the Cemani population. Thus, this briefly genotyping method effectively maintains and protects the pure line of Cemani chicken.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Dharmayanthi, A. B., Kinoshita, K., Khaerunnisa, I., Safitry, R. S., Iryanto, S. B., Yohanna,, Sutikno,, Ishak, A. B. L., Zein, M. S. A., Satta, Y., Akiyama, T., Sumantri, C.. 2022-11-15. Identification of variation in Fibromelanosis region on chromosome 20 for determining the purity of Indonesian Cemani chicken. https://doi.org/10.1101/2022.11.13.516295

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Large language model-based bibliometric evaluation of population descriptors in human genetics

As the use of population descriptors such as race, ethnicity, and ancestry have become increasingly common in modern genetics research, there have been growing calls to critically examine their use. Most notably, in 2023, the National Academies of Science, Engineering, and Medicine (NASEM) published a report titled Using Population Descriptors in Genetics and Genomics Research: A New Framework for an Evolving Field, which included eight specific and actionable recommendations for researchers to implement the ethical and accurate use of population descriptors in genetic research. Here, we use the 2023 NASEM report as a benchmark to analyze the use of population descriptors in genome-wide association studies (GWAS). We develop a general toolkit for large language model-based bibliometrics, operationalize the report's recommendations into an evaluation framework, and apply this framework to evaluate all 4,007 papers from the GWAS Catalog published between 2007 and 2025 with full text available on PubMedCentral. We find significant improvements in adherence to NASEM report recommendations over time. However, most improvements predate the publication of the NASEM report itself, suggesting the report functioned primarily as a synthesis of existing best practices rather than a catalyst for change. We conclude by highlighting opportunities for growth in the field of human genetics.

genetics↗

Mitigating biases of rescaling in forward-in-time population genetic simulations

Forward-in-time population genetic simulations are widely used in evolutionary analyses, but simulating large populations and long genomic regions remains computationally demanding. To reduce this cost, parameter rescaling is widely employed, in which the original evolutionary process is approximated by one with a smaller population size and fewer generations. Recently, several studies using the SLiM simulator have raised concerns about the accuracy of this rescaling approach. In this study, we show that many of the biases reported in these studies can be mitigated by using a different simulation algorithm. These results reveal that the accuracy of parameter rescaling depends on how well the simulation algorithm preserves diffusion-limit properties under rescaling.

genetics↗

OPA1 controls mitochondrial dysfunction-driven liver fibrosis in MASLD

Progressive hepatic fibrosis is the principal determinant of morbidity and mortality in metabolic dysfunction-associated steatotic liver disease and steatohepatitis (MASLD/MASH). Mitochondrial dysfunction is a hallmark of MASH, and the release of mitochondrial damage-associated molecular patterns (mito-DAMPs) from injured hepatocytes can promote fibrosis. However, how mitochondrial dynamics and quality control shape the fibrotic response in MASLD/MASH remains unclear. Here, through large-scale genomic analyses of mitochondrial genes governing mitophagy, fusion and fission in human MASLD, with a power-equivalent sample size of approximately 700,000 individuals, we identify a strong association between hepatic fibrosis and the mitochondrial fusion factor dynamin-like GTPase optic atrophy 1 (OPA1). OPA1 transcripts and protein abundance in the liver epithelium were progressively dysregulated with advancing fibrosis. In mice, hepatocyte-specific OPA1 loss alone was sufficient to induce hepatic stellate cell activation and fibrosis in zone 3, promoted the release of mito-DAMPs into the circulation and exacerbated fibrosis in experimental MASH. These findings identify OPA1 as a central regulator of the hepatic fibrotic response and connect defective mitochondrial homeostasis to mito-DAMP release, hepatic stellate cell activation and fibrosis in MASLD.

genetics↗