Fbxw17 is dispensable for viability and fertility in mice

Chen, Zhen; Ma, Dupeng; Jin, Tingyu; Yu, Ziqi; Li, Jiong; Sun, Qi; Li, Zejia; Du, Ziye; Liu, Rong; Li, Yi; Luo, Mengcheng

doi:10.1007/s11033-022-07512-z

Cited by 4 publications

(3 citation statements)

References 43 publications

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“…The reproductive parameter results indicated that Fbxo22 is not required for spermatogenesis or male fertility. Currently, research findings suggest that numerous genes encoding ubiquitin enzymes expressed in the testis are not necessary for mouse fertility (e.g., ankyrin repeat and SOCS box containing 12 (Asb12) [25], Asb15 [26], F-box and WD-40 domain protein 17 (Fbxw17) [27]). Our findings eliminate Fbxo22 as a target for contraception and as a factor in male infertility, which can prevent redundant research efforts and save resources in other laboratories.…”

Section: Discussionmentioning

confidence: 99%

E3 ligase FBXO22 is not significant for spermatogenesis and male fertility in mice

2024

Am J Transl Res

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Background: F-box-only protein 22 (FBXO22), an important substrate receptor of the SKP1-Cullin-F-box (SCF) ubiquitin ligases, has been reported to be involved in many biological processes, including tumorigenesis, neurological disorders, cellular senescence, and DNA damage. However, the specific role of FBXO22 during spermatogenesis is poorly understood. Methods: We produced Fbxo22 conditional knockout (cKO) and global knockout (KO) mice and assessed their sperm masurements using a computer-assisted sperm analysis (CASA) system. Additionally, we conducted histologic staining and immunostaining to examine the impact of Fbxo22 loss on spermatogenesis. Results: Our results revealed that there were no notable differences in semen quality, fertility test results, or histologic findings in Fbxo22-KO and Fbxo22-cKO mice compared to the control group. Conclusions: Our study demonstrated that Fbxo22 is not significant for spermatogenesis or male fertility in mice. These findings will help researchers avoid redundant efforts and serve as a foundational resource for genetic studies on human fertility.

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Section: Discussionmentioning

confidence: 99%

E3 ligase FBXO22 is not significant for spermatogenesis and male fertility in mice

2024

Am J Transl Res

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“…At present, study findings indicate that many genes expressed in the testis are dispensable for mouse fertility ( e.g ., FBXW17 ( Chen et al, 2022b ), ASB12 ( Zhang et al, 2022 ), USP26 ( Felipe-Medina et al, 2019 )). Our results exclude SLC26A1 as a contraceptive target and male infertility factor and will help avoid duplication of effort by researchers and save time and money in other laboratories.…”

Section: Discussionmentioning

confidence: 99%

Slc26a1 is not essential for spermatogenesis and male fertility in mice

Meng,

Qiao,

Xue

et al. 2023

PeerJ

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Thousands of genes are expressed in the testis of mice. However, the details about their roles during spermatogenesis have not been well-clarified for most genes. The purpose of this study was to examine the effect of Slc26a1 deficiency on mouse spermatogenesis and male fertility. Slc26a1-knockout (KO) mice were generated using CRISPR/Cas9 technology on C57BL/6J background. We found no obvious differences between Slc26a1-KO and Slc26a1-WT mice in fertility tests, testicular weight, sperm concentrations, or morphology. Histological analysis found that Slc26a1-KO mouse testes had normal germ cell types and mature sperm. These findings indicated that Slc26a1 was dispensable for male fertility in mice. Our results may save time and resources by allowing other researchers to focus on genes that are more meaningful for fertility studies. We also found that mRNAs of two Slc26a family members (Slc26a5 and Slc26a11) were expressed on higher mean levels in Slc26a1-KO total mouse testes, compared to Slc26a1-WT mice. This effect was not found in mouse GC-1 and GC-2 germ cell lines with the Slc26a1 gene transiently knocked down. This result may indicate that a gene compensation phenomenon was present in the testes of Slc26a1-KO mice.

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“…Subsequently, the protein samples were mixed with SDS sample loading buffer, boiled for 10 minutes, and separated using 10% SDS-PAGE. The obtained proteins were transferred onto a PVDF membrane, and immunoblotting assays were conducted following established protocols [20]. The primary antibodies employed were rabbit anti-TEX2 (1:500, 12774-1-AP, Proteintech) and mouse anti-α-Tubulin (1:2000, ab4074, Abcam).…”

Section: Western Blottingmentioning

confidence: 99%

Investigating the role of a testis-expressed gene Tex2 in spermatogenesis in mice

Wang,

Li,

Shen

et al. 2024

Preprint

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Background Although TEX2 is primarily expressed in the testes of mammals, its exact role in reproduction remains unclear. This study aims to explore whether TEX2 plays a role in determining fertility in mice. Methods To address this issue, a mouse model with Tex2 knockout was created through CRISPR/Cas9 technology. Various experiments, including qPCR, Western blotting, immunofluorescence, electron microscopy, CASA, and H&E staining, were conducted to evaluate the role of TEX2 on mouse spermatogenesis. Results Although a percentage of spermatozoa exhibited defects in morphology and motility following Tex2 knockout, these abnormalities had no significant impact on the fertility of male mice. Additionally, the knockout did not significantly influence ovarian development or oogenesis in female mice. Conclusions In summary, despite the deletion of Tex2 having a minor impact on spermatogenesis in mice, it did not significantly affect their overall fertility. It is possible that alternative mechanisms might compensate for the absence of Tex2, or that Tex2 has a dispensable role in the reproductive process. This discovery offers a fresh outlook on the genetic regulatory mechanisms involved in the reproductive process, potentially catalyzing further investigations in related fields.

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Fbxw17 is dispensable for viability and fertility in mice

Cited by 4 publications

References 43 publications

E3 ligase FBXO22 is not significant for spermatogenesis and male fertility in mice

E3 ligase FBXO22 is not significant for spermatogenesis and male fertility in mice

Slc26a1 is not essential for spermatogenesis and male fertility in mice

Investigating the role of a testis-expressed gene Tex2 in spermatogenesis in mice

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