QTL for the heritable inverted teat defect in pigs

Jonas, Elisabeth; Schreinemachers, H.-J.; Kleinwächter, Tina; Ün, Cemal; Oltmanns, Ina; Tetzlaff, Sylvio; Jennen, Danyel; Tesfaye, D.; Ponsuksili, Siriluck; Muráni, Eduard; Juengst, H.; Tholen, Ernst; Schellander, K.; Wimmers, Klaus

doi:10.1007/s00335-007-9086-5

Cited by 27 publications

(37 citation statements)

References 48 publications

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“…The average number of inverted teats in affected pigs in our study was 3.1, which is similar to the figures presented in earlier studies in different commercial pig lines (Beilage et al 1996; Clayton et al 1981; Hittel 1984; Jonas et al 2008; Mayer and Pirchner 1995). The study of a larger Swedish Yorkshire cohort reported that in 2010, 13% of the Swedish Yorkshire animals with potential for breeding did have at least one inverted teat at the time point of selection (Chalkias et al 2013).…”

Section: Resultssupporting

confidence: 92%

“…The positions of previously reported QTL for teat traits were compared to our findings. Previously, some of the results shown here had been combined with data from a linkage study (Jonas et al 2008). Microsatellite markers which had not been mapped to the ENSEMBL genome in that study were further located using flanking markers according to the NCBI map-viewer (http://www.ncbi.nlm.nih.gov/projects/mapview/maps.cgi?).…”

Section: Methodsmentioning

confidence: 89%

“…There have been only a few studies on genetic markers for the inverted teat defect or other teat abnormalities in pigs. Quantitative trait loci (QTLs) have previously been reported on different chromosomes for inverted teats (Jonas et al 2008) and for extremely small teats (Sato et al 2006), while expression studies were performed for the inverted teat (Chomwisarutkun et al 2012a, b, 2013). The region identified on chromosome 2 overlapped to both the previous linkage studies (Jonas et al 2008; Sato et al 2006) and the expression study (Chomwisarutkun et al 2012b).…”

Section: Resultsmentioning

confidence: 99%

“…Presently, only a few studies have focused on the identification of genetic regions associated with this trait, using linkage and expression analysis (Chomwisarutkun et al 2012a, b; Jonas et al 2008). A number of candidate genes had been tested, including parathyroid hormone-like hormone gene ( PTHLH ) and its receptor ( PTHR1 ), which have been suggested as possible regulators for inverted teats (Tetzlaff et al 2009).…”

Section: Introductionmentioning

confidence: 99%

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Identification of novel candidate genes for the inverted teat defect in sows using a genome-wide marker panel

et al. 2017

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The number of functional teats is an important selection criterion in pig breeding. Inherited defects of the udder, such as the inverted teat, do have a considerable negative impact on the nursing ability of the sow. To investigate the genetic background of this defect and the number of functional teats in Swedish maternal lines, samples from 230 Yorkshire pigs were selected for genotyping using the PorcineSNP60K BeadChip (Illumina Inc.), each pig with at least one inverted teat was matched with one non-affected pig (fullsib or pairs with matching herd and gender). A genome-wide association study on these 230 pigs was performed using the two-step approach implemented in GenABEL using 46,652 single nucleotide polymorphisms across all autosomes and the X chromosome. A number of significant regions were identified for the inverted teat defect on chromosomes 2, 10, and 18. Many of the regions associated with the number of functional teats were located in the same or close regions, except two associated markers on the X chromosome and one on chromosome 3. We identified some of the regions on chromosomes previously reported in one linkage and one gene expression study. We conclude, despite being able to suggest new candidate genes, that further studies are needed to better understand the biologic background of the teat development. Despite the in-depth comparison of identified regions for the inverted teat defect done here, more studies are required to allow a clear identification of genetic regions relevant for this defect across many pig populations.Electronic supplementary materialThe online version of this article (doi:10.1007/s13353-016-0382-1) contains supplementary material, which is available to authorized users.

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Section: Resultssupporting

confidence: 92%

Section: Methodsmentioning

confidence: 89%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Identification of novel candidate genes for the inverted teat defect in sows using a genome-wide marker panel

et al. 2017

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“…As to its expansive role in mammary gland development, LEF-1 gene was identified as a candidate gene for teat number trait (Jonas et al, 2008; Tetzlaff et al, 2009). We tested the levels of LEF-1 mRNA in different tissues and the mammary gland at different developmental stages and found extremely high levels in the teat that had a tendency to gradually decrease during growth which suggested its enormous regulatory potential in mammary gland development.…”

Section: Introductionmentioning

confidence: 99%

Association of Novel Polymorphisms in Lymphoid Enhancer Binding Factor 1 (LEF-1) Gene with Number of Teats in Different Breeds of Pig

Xu¹,

Wei²,

Wang³

et al. 2014

Asian Australas. J. Anim. Sci

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Lymphoid enhancer binding factor 1 (LEF-1) is a member of the T-cell specific factor (TCF) family, which plays a key role in the development of breast endothelial cells. Moreover, LEF-1 gene has been identified as a candidate gene for teat number trait. In the present study, we detected two novel mutations (NC_010450.3:g. 99514A>G, 119846C>T) by DNA sequencing and polymerase chain reaction-restriction fragment length polymorphism in exon 4 and intron 9 of LEF-1 in Guanzhong Black, Hanjiang Black, Bamei and Large White pigs. Furthermore, we analyzed the association between the genetic variations with teat number trait in these breeds. The 99514A>G mutation showed an extremely significant statistical relevance between different genotypes and teat number trait in Guanzhong (p<0.001) and Large White (p = 0.002), and significant relevance in Hanjiang (p = 0.017); the 119846C>T mutation suggested significant association in Guanzhong Black pigs (p = 0.042) and Large White pigs (p = 0.003). The individuals with “AG” or “GG” genotype displayed more teat numbers than those with “AA”; the individuals with “TC” or “CC” genotype showed more teat numbers than those with “TT”. Our findings suggested that the 99514A>G and 119846C>T mutations of LEF-1 affected porcine teat number trait and could be used in breeding strategies to accelerate porcine teat number trait improvement of indigenous pigs breeds through molecular marker assisted selection.

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A variant in long noncoding RNA NORSF affects granulosa cells response to transcription factor RFX7

Wang,

Zhang,

Sheng

et al. 2024

Journal Cellular Physiology

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NORSF is a nuclear long noncoding RNA (lncRNA) that contributes to the follicular atresia and restrains 17β‐estradiol (E2) release by granulosa cells (GCs). Importantly, it is also a potential candidate gene in the quantitative trait locus (QTLs) for sow fertility traits. We identified NORSF as a candidate (causal) gene affecting sow fertility traits. A novel G–A variant was discovered at −478 nt of the NORSF promoter and termed as g.−478G>A. Association analysis revealed that this variant was associated with sow fertility traits (e.g., the total number of piglets born, the total number of piglets born alive, and the number of healthy piglets). Mechanistically, the g.−478G>A variant reduced the binding activity of the NORSF promoter to its transcription activator regulatory factor X7 (RFX7), leading to decreased NORSF promoter activity and transcription levels in sow GCs (sGCs), and weakened inhibitory effects on the transcription of CYP19A1, which encodes a rate‐limiting enzyme for E2 synthesis and E2 release by sGCs. In addition, RFX7 is transcriptionally activated by P53, which restrains E2 release from sGCs via the RFX7/NORSF/CYP19A1 pathway. These findings indicate that the lncRNA NORSF is a causal gene in QTLs for sow fertility traits and define the P53/NORSF/CYP19A1 pathway as a new signaling pathway affecting sow reproduction, which provides a new target for improving female fertility.

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QTL for the heritable inverted teat defect in pigs

Cited by 27 publications

References 48 publications

Identification of novel candidate genes for the inverted teat defect in sows using a genome-wide marker panel

Identification of novel candidate genes for the inverted teat defect in sows using a genome-wide marker panel

Association of Novel Polymorphisms in Lymphoid Enhancer Binding Factor 1 (LEF-1) Gene with Number of Teats in Different Breeds of Pig

A variant in long noncoding RNA NORSF affects granulosa cells response to transcription factor RFX7

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