Zrsr2-KO Mouse
一般名
Zrsr2-KO
製品ID
S-KO-17795
背景情報
C57BL/6JCya
系統ID
KOCMP-22184-Zrsr2-B6J-VB
状況
このマウス系統を論文で使用する場合は、「Zrsr2-KO Mouse(カタログ番号S-KO-17795)はサイアジェンから購入しました。」と引用してください。
製品タイプ
年齢
遺伝子型
性別
数量
標準的な配送方法では、少なくとも3匹のヘテロ接合体キャリアを保証しています。ホモ接合体キャリアや指定された性別の個体の繁殖サービスも利用可能です。
基本情報
系統名
Zrsr2-KO
系統ID
KOCMP-22184-Zrsr2-B6J-VB
遺伝子名
製品ID
S-KO-17795
遺伝子別名
URP, 35kDa, U2af1-rs2, 5031411E02Rik, A230052C13Rik
遺伝子別名
C57BL/6JCya
NCBI ID
修正
Conventional knockout
染色体
Chr X
表現型
アプリケーション
--
さらに
系統詳細
EnsemblトランスクリプトID
ENSMUST00000112289
NCBIトランスクリプトID
NM_009453
ターゲット領域
Exon 3
有効領域の大きさ
~1.2 kb
遺伝子研究の概要
Zrsr2, zinc finger CCCH-type, RNA binding motif and serine/arginine rich 2, is an essential splicing factor. As a component of both the major and minor spliceosomes, it is involved in 3' splice-site recognition, mediating the splicing of U2-type (major) and U12-type (minor) introns. It plays a significant role in multiple biological processes, and genetic models such as gene-knockout mouse models are valuable for studying its functions [2].
In mouse models, Zrsr2 mutant lines showed blood cell anomalies, and in some lines, oogenesis was blocked at the secondary follicle stage. RNA-seq of Zrsr2 mutant secondary follicles indicated aberrant gene expression and altered alternative splicing events, with enrichment of U12-type intron retention. These events were related to centriole replication, protein phosphorylation, and DNA damage checkpoint, and AS events of 50 meiotic genes were also affected, suggesting Zrsr2 mutations can impede oogenesis and female fertility [1].
In zebrafish, zrsr2-knockout embryos displayed multiple developmental defects starting at 4 days post-fertilization and died after 8 dpf, and the loss of Zrsr2 led to down-regulation of essential metabolic pathways and aberrant retention of minor introns in about one-third of all minor intron-containing genes [2].
In mice with concurrent Zrsr2 mutation and Tet2 loss, it promoted myelodysplastic neoplasm (MDS), presenting peripheral blood cytopenia, splenomegaly, extramedullary hematopoiesis, and multi-lineage dysplasia. Whole-transcriptome analysis in HSPC revealed key alterations in ribosome, inflammation, and migration/motility processes, and the MAPK pathway was the most affected target by mRNA aberrant splicing [3].
In conclusion, Zrsr2 is crucial for the splicing of U12-type introns and is essential for various biological processes such as embryonic development, follicular development, and hematopoiesis. The use of gene-knockout mouse models and other genetic models has significantly contributed to understanding its role in diseases like MDS and its impact on female fertility and embryonic development.
References:
1. Gómez-Redondo, Isabel, Pericuesta, Eva, Navarrete-Lopez, Paula, Horiuchi, Keiko, Gutiérrez-Adán, Alfonso. 2022. Zrsr2 and functional U12-dependent spliceosome are necessary for follicular development. In iScience, 25, 103860. doi:10.1016/j.isci.2022.103860. https://pubmed.ncbi.nlm.nih.gov/35198906/
2. Weinstein, Rachel, Bishop, Kevin, Broadbridge, Elizabeth, Bresciani, Erica, Sood, Raman. 2022. Zrsr2 Is Essential for the Embryonic Development and Splicing of Minor Introns in RNA and Protein Processing Genes in Zebrafish. In International journal of molecular sciences, 23, . doi:10.3390/ijms231810668. https://pubmed.ncbi.nlm.nih.gov/36142581/
3. Garcia-Ruiz, Cristian, Martínez-Valiente, Cristina, Cordón, Lourdes, Gutiérrez-Adán, Alfonso, Sanjuan-Pla, Alejandra. 2022. Concurrent Zrsr2 mutation and Tet2 loss promote myelodysplastic neoplasm in mice. In Leukemia, 36, 2509-2518. doi:10.1038/s41375-022-01674-2. https://pubmed.ncbi.nlm.nih.gov/36030305/
品質管理基準
精子検査
凍結前の精子濃度を測定し、精子の生存能力の判定します。
凍結後の精子では、各バッチから1本の凍結保存された精子を選び出し、体外受精に使用します。
環境基準:
SPF対応地域:
グローバル由来:
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