Rpl7l1-KO Mouse

Rpl7l1, 60S Ribosomal Protein L7-Like 1, is associated with ribosome biogenesis, which is crucial for protein synthesis and cell growth. It has been linked to mouse embryonic development, skeletal muscle, and is involved in pathways related to cell differentiation and the cell cycle [1,4,5]. Genetic models, like mouse models, are valuable for studying its functions.

Functional knockdown of Rpl7l1 in mouse preimplantation embryos led to normal morula development but failure to form a blastocoel cavity or differentiated trophectoderm, indicating its requirement for blastocyst formation [5]. In a pan-cancer study, Rpl7l1 was overexpressed in nine tumor types. Its gene mutation, tumor microenvironment, and methylation modification play key roles in patient prognosis, and high expression was associated with TMB, MSI, LOH especially in LIHC and HNSC. Experimental verification showed it can promote tumor cell proliferation and migration [1]. In pigs, Rpl7l1 was identified as a hub gene in a protein-protein interaction network related to abdominal subcutaneous fat deposition, and was a potential obese-specific biomarker [2]. In lung adenocarcinoma, it was among hub genes overexpressed and enriched in RNA processing, ribosome biogenesis, and mitochondrial translation, with high-expression cohorts having poor overall survival [3].

In conclusion, Rpl7l1 is essential for mammalian blastocyst formation. In disease-related studies, its abnormal expression in cancer and potential role in fat deposition in pigs suggest its significance in oncology and obesity-related research. Mouse models have been instrumental in uncovering these functions, providing insights into the underlying biological mechanisms and potential therapeutic targets in these disease areas.

References:

1. He, Ke-Jie, Gong, Guoyu, Liang, E, Lin, Shuiquan, Xu, Jianguang. 2023. Pan-cancer analysis of 60S Ribosomal Protein L7-Like 1 (RPL7L1) and validation in liver hepatocellular carcinoma. In Translational oncology, 40, 101844. doi:10.1016/j.tranon.2023.101844. https://pubmed.ncbi.nlm.nih.gov/38042135/

2. Yang, Yongli, Wang, Xiaoyi, Li, Mingli, Chen, Qiang, Lu, Shaoxiong. 2024. Identification of potential obese-specific biomarkers and pathways associated with abdominal subcutaneous fat deposition in pig using a comprehensive bioinformatics strategy. In PeerJ, 12, e17486. doi:10.7717/peerj.17486. https://pubmed.ncbi.nlm.nih.gov/38832038/

3. Mukherjee, Arnab, Boonbangyang, Manon, K S, Mukunthan. 2025. Unraveling the intricate molecular landscape and potential biomarkers in lung adenocarcinoma through integrative epigenomic and transcriptomic profiling. In Scientific reports, 15, 9154. doi:10.1038/s41598-025-93769-w. https://pubmed.ncbi.nlm.nih.gov/40097569/

4. Mishra, Manish, Kane, Alice E, Young, Alexander P, Howlett, Susan E. 2022. Age, sex, and frailty modify the expression of common reference genes in skeletal muscle from ageing mice. In Mechanisms of ageing and development, 210, 111762. doi:10.1016/j.mad.2022.111762. https://pubmed.ncbi.nlm.nih.gov/36509213/

5. Maserati, Marc, Dai, Xiangpeng, Walentuk, Melanie, Mager, Jesse. 2012. Identification of four genes required for mammalian blastocyst formation. In Zygote (Cambridge, England), 22, 331-9. doi:10.1017/S0967199412000561. https://pubmed.ncbi.nlm.nih.gov/23211737/