Financing & Policy

Evidence brief: Development and validation of a simple, cost-effective competitive allele-specific PCR assay for largescale screening and detection of FecB mutation in sheep

A sourced PLOS One study, published 2025-12-02. Read the researchers’ findings, methods and context, with links to connected African health evidence.

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Published in PLOS One on 2025-12-02, this study is presented as an attributed evidence briefing. The excerpts below are the original researchers’ words, reproduced under their Creative Commons Attribution licence. Health Signal has selected the abstract and, where needed, opening background paragraphs; the complete methods, results, limitations and references remain in the linked paper.

Original authors: Kathiravan Periasamy, Rudolf Pichler, Saravanan Ramasamy, Rajesh Kumar Somasundaram, Muladno Basar, Atanaska Teneva, Amadou Traore, Arnaud S R Tapsoba, Mohammed O Faruque, Seyed Abbas Rafat, Tanveer Hussain

Source: PLOS One • DOI 10.1371/journal.pone.0337392

Read the complete primary study ↗ · Creative Commons Attribution licence

From the researchers

Abstract

The Booroola fecundity (FecB) gene, a mutation in the bone morphogenetic protein receptor-1B (BMPR1B), is known to increase ovulation rate and litter size in sheep. Efficient and accurate, large-scale detection of this single nucleotide polymorphism (SNP) is critical for marker assisted introgression/selection programs for genetic improvement of prolificacy. This study aimed to develop and validate a robust, cost-effective, and high-throughput genotyping assay for detecting the FecB mutation across diverse sheep populations globally. A competitive allele-specific PCR (KASP) assay targeting the A746G nucleotide substitution in BMPR1B gene was designed and tested on a diverse panel of 224 individuals across 22 sheep breeds and validated against direct sequencing. The KASP genotyping results showed 100% concordance with sequence data, with clear fluorescence-based discrimination of homozygous wild-type Fec++ (AA), heterozygous FecB+ (AG), and homozygous mutant FecBB (GG) genotypes. The assay was compatible across three real-time PCR platforms, BioRad CFX96, Roche LightCycler 480 II, and ABI QuantStudio 6 demonstrating reproducible genotyping and cross-platform interoperability. Subsequently, the KASP assay was applied to a global screening of 1471 sheep from 47 breeds in 14 countries for further validation of the assay. The mutation was not observed in the sheep samples investigated from Africa, Europe, Latin America, and West Asia, whereas it was polymorphic or fixed in certain populations from South (India and Bangladesh) and Southeast Asia (Indonesia). Notably, native Bangladeshi sheep exhibited high frequencies of the FecB allele, with some populations (e.g., Bangladesh Central) nearing fixation, reflecting possible selection for high prolificacy. In conclusion, the validated KASP assay offers a powerful, scalable tool for the rapid genotyping of the FecB mutation, enabling efficient screening and incorporation of prolificacy traits in sheep breeding programs worldwide.

Introduction

Prolificacy, defined by the ability to produce multiple offsprings per birth, is a critical trait with significant implications on the efficiency and productivity of sheep farming. Higher prolificacy with more number of lambs born per ewe/year can significantly enhance overall flock productivity [1]. For smallholder farmers, who often operate with limited resources and land, higher prolificacy translates directly into increased flock size and enhanced meat production per breeding cycle [2]. This increased productivity can significantly boost household income and food security, allowing smallholders to maximize returns on their investment in feed, labour and veterinary care. Additionally, sheep breeds with high prolificacy can contribute to rapid genetic improvements within flocks, as more offspring provide more selection opportunities for desirable traits.

The FecB (Booroola) mutation in sheep has garnered significant attention due to its profound impact on prolificacy. FecB mutation is a single nucleotide polymorphism in the BMPR1B (Bone Morphogenetic Protein Receptor 1B) gene that plays a critical role in regulating ovulation rates and litter size [3]. The substitution (A746G) in exon 8 of the BMPR1B gene leads to an amino acid change (Q249R) that alters receptor activity and disrupts the normal inhibitory signalling pathway of bone morphogenetic proteins in granulosa cells. This functional alteration induces maturation of ovarian follicles by increasing the sensitivity of the follicles to Follicle Stimulating Hormone (FSH), thus resulting in higher ovulation rate and litter size. The weighted mean advantage of ewes carrying one copy of FecB mutation was estimated to be + 1.3 (range +0.8 to +2.0) for ovulation rate and +0.7 (range +0.4 to +1.3) for litter size across different production systems and varying recipient genetic background [1]. As the use of sheep carrying the FecB gene offers a substantial increase in fecundity in one generation, crossing experiments have been undertaken in several countries to evaluate and introgress FecB into other breeds [1]. Large-scale introgression and marker-assisted selection efforts have successfully incorporated the FecB allele into low-prolific breeds demonstrating substantial gains in lambing percentage and reproductive efficiency under diverse production systems. This mutation’s ability to significantly boost fecundity makes it a valuable genetic marker for breeding programs aimed at improving reproductive efficiency in various sheep breeds.

Reading this evidence

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This briefing makes the source accessible within the wider financing & policy desk. It does not assess an individual patient or certify a product. When considering relevance to another health system, examine the original authors’ account of context and limitations, then seek local implementation evidence. The related reporting below provides other studies to read alongside this one; it is a topic connection, rather than a claim that their results are directly comparable.

© 2025 Kathiravan Periasamy, Rudolf Pichler, Saravanan Ramasamy, Rajesh Kumar Somasundaram, Muladno Basar, Atanaska Teneva, Amadou Traore, Arnaud S R Tapsoba, Mohammed O Faruque, Seyed Abbas Rafat, Tanveer Hussain. Excerpts reproduced under CC BY. Selection, formatting and contextual notes by Health Signal. The researchers are the authors of the source study, not members of Health Signal’s staff.

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Health Signal’s publication desk curates source-based health analysis and attributed research briefings. Study authors and originating institutions are credited within each article. Preparation used AI assistance; source and licence checks do not constitute independent replication or clinical endorsement.

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