A nonsense mutation in the <i>FGF5</i> gene is associated with the long‐haired phenotype in domestic guinea pigs (<i>Cavia porcellus</i>)

Yu, Feng; Liu, Zhengxi; Jiao, Shuyu; Zhang, Xiaoying; Bai, Chen; Zhang, Jiabao; Yan, Shouqing

doi:10.1111/age.12656

Cited by 5 publications

(3 citation statements)

References 5 publications

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“…A missense mutation in FGF5 was found in longhaired cats (Drögemüller et al, 2007 ; Kehler et al, 2007 ). The long-hair phenotype of FGF5 gene knockout or mutations has also been reported in sheep, goat, donkey, hamster and guinea pigs (Legrand et al, 2014 ; Wang et al, 2015 , 2016 ; Yoshizawa et al, 2015 , 2016 ; Hu et al, 2017 ; Li et al, 2017 ; Yu et al, 2018 ). These findings provide evidence that FGF5 functions as an inhibitor of hair elongation, thus identifying one of the FGF5 key functions.…”

Section: Discussionmentioning

confidence: 86%

FGF5 Regulates Schwann Cell Migration and Adhesion

Chen

Hu²,

et al. 2020

Front. Cell. Neurosci.

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The fibroblast growth factor (FGF) family polypeptides play key roles in promoting tissue regeneration and repair. FGF5 is strongly up-regulated in Schwann cells of the peripheral nervous system following injury; however, a role for FGF5 in peripheral nerve regeneration has not been shown up to now. In this report, we examined the expression of FGF5 and its receptors FGFR1-4 in Schwann cells of the mouse sciatic nerve following injury, and then measured the effects of FGF5 treatment upon cultured primary rat Schwann cells. By microarray and mRNA sequencing data analysis, RT-PCR, qPCR, western blotting and immunostaining, we show that FGF5 is highly up-regulated in Schwann cells of the mouse distal sciatic nerve following injury, and FGFR1 and FGFR2 are highly expressed in Schwann cells of the peripheral nerve both before and following injury. Using cultured primary rat Schwann cells, we show that FGF5 inhibits ERK1/2 MAP kinase activity but promotes rapid Schwann cell migration and adhesion via the upregulation of N-cadherin. Thus, FGF5 is an autocrine regulator of Schwann cells to regulate Schwann cell migration and adhesion.

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Section: Discussionmentioning

confidence: 86%

FGF5 Regulates Schwann Cell Migration and Adhesion

Chen

Hu²,

et al. 2020

Front. Cell. Neurosci.

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“…A spontaneous mutation in the FGF5 gene was first discovered in angora mice, which have a 50% longer hair coat length compared with that of the wild‐type mice (Hébert et al, 1994). Then, several studies on the FGF5 gene demonstrated the relation to coat hair length in cats (Drögemüller et al, 2007; Shaffer et al, 2021), dogs (Dierks et al, 2013), humans (Higgins et al, 2014), donkeys (Legrand et al, 2014), hamsters (Yoshizawa et al, 2015), llamas (Daverio et al, 2017), guinea pigs (Yu et al, 2018), alpacas (Pallotti et al, 2018a,b), sheep (Zhang et al, 2019), and dromedary (Maraqa et al, 2021). It is currently regarded that FGF5 is overexpressed during the late anagen phase and serves as a crucial regulatory factor that promotes the anagen‐to‐catagen transition in the hair follicle cycle (Suzuki et al, 1998; Ota et al, 2002; He et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

A deletion variant within the FGF5 gene in goats is associated with gene expression levels and cashmere growth

Song

Zhang

et al. 2022

Animal Genetics

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The FGF5 gene has been associated with the regulation of fibre length in mammals, including cashmere goats. A deletion variant at ~14 kb downstream of the FGF5 gene showed significant divergence between cashmere and non‐cashmere goats in previous studies. In this study, we designed specific primers to genotype the deletion variant. The results of gel electrophoresis and Sanger sequencing revealed that a 507‐bp deletion mutation is located at 95 454 685–95 455 191 of chromosome 6 in goats. Genotyping data from a large panel of 288 goats showed that the deletion at the FGF5 gene locus appeared to be associated with cashmere length. The deletion variant was close to fixation (frequency 0.97) in cashmere goats. Furthermore, electrophoretic mobility shift assays for evaluating DNA–protein interaction and mRNA expression levels of FGF5 suggested that the deletion variant may serve as a cis‐acting element by specifically binding transcription factors to mediate quantitative changes in FGF5 mRNA expression. Our study illustrates how a structural mutation of the FGF5 gene has contributed to the cashmere growth phenotype in domestic goats. The deletion mutation within the FGF5 gene could potentially serve as a molecular marker of cashmere growth in cashmere goat breeding.

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“…Mutations in the FGF5 gene form the genetic basis for familial trichomegaly, which is manifested as increased hair growth and abnormally long and thick eyelashes for the carriers of the mutated FGF5 gene. FGF5-deficient or knockout animals (including mice, sheep, cats, dogs and guinea pigs) also have abnormally thick and long hair ( Yu et al, 2018 ). A previous study has shown that an FGF5-derived decapeptide that possesses FGF5-antagonizing activity can promote hair growth in mice ( Ito et al, 2003 ).…”

Section: Introductionmentioning

confidence: 99%

Suppression of FGF5 and FGF18 Expression by Cholesterol-Modified siRNAs Promotes Hair Growth in Mice

et al. 2021

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FGF5 and FGF18 are key factors in the regulation of the hair follicle cycle. FGF5 is overexpressed during the late anagen phase and serves as a crucial regulatory factor that promotes the anagen-to-catagen transition in the hair follicle cycle. FGF18, which is overexpressed during the telogen phase, mainly regulates the hair follicle cycle by maintaining the telogen phase and inhibiting the entry of hair follicles into the anagen phase. The inhibition of FGF5 may prolong the anagen phase, whereas the inhibition of FGF18 may promote the transition of the hair follicles from the telogen phase to the anagen phase. In the present study, we used siRNA to suppress FGF5 or FGF18 expression as a way to inhibit the activity of these genes. Using qPCR, we showed that FGF5-targeting siRNA modified by cholesterol was more effective than the same siRNA bound to a cell-penetrating peptide at suppressing the expression of FGF5 both in vitro and in vivo. We then investigated the effects of the cholesterol-modified siRNA targeting either FGF5 or FGF18 on the hair follicle cycle in a depilated area of the skin on the back of mice. The cholesterol-modified siRNA, delivered by intradermal injection, effectively regulated the hair follicle cycle by inhibiting the expression of FGF5 and FGF18. More specifically, intradermal injection of a cholesterol-modified FGF5-targeted siRNA effectively prolonged the anagen phase of the hair follicles, whereas intradermal injection of the cholesterol-modified FGF18-targeted siRNA led to the mobilization of telogen follicles to enter the anagen phase earlier. The inhibitory effect of the cholesterol-modified FGF18-targeted siRNA on FGF18 expression was also evaluated for a topically applied siRNA. Topical application of a cream containing the cholesterol-modified FGF18-targeted siRNA on a depilated area of the skin of the back of mice revealed comparable inhibition of FGF18 expression with that observed for the same siRNA delivered by intradermal injection. These findings suggested that alopecia could be prevented and hair regrowth could be restored either through the intradermal injection of cholesterol-modified siRNA targeting FGF5 or FGF18 or the topical application of FGF18 siRNA.

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A nonsense mutation in the FGF5 gene is associated with the long‐haired phenotype in domestic guinea pigs (Cavia porcellus)

Cited by 5 publications

References 5 publications

FGF5 Regulates Schwann Cell Migration and Adhesion

FGF5 Regulates Schwann Cell Migration and Adhesion

A deletion variant within the FGF5 gene in goats is associated with gene expression levels and cashmere growth

Suppression of FGF5 and FGF18 Expression by Cholesterol-Modified siRNAs Promotes Hair Growth in Mice

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