C57BL/6JCya-Myo19em1flox/Cya
Common Name:
Myo19-flox
Product ID:
S-CKO-12937
Background:
C57BL/6JCya
Product Type
Age
Genotype
Sex
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Basic Information
Strain Name
Myo19-flox
Strain ID
CKOCMP-66196-Myo19-B6J-VA
Gene Name
Product ID
S-CKO-12937
Gene Alias
1110055A02Rik; Myohd1
Background
C57BL/6JCya
NCBI ID
Modification
Conditional knockout
Chromosome
11
Phenotype
Document
Application
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Note: When using this mouse strain in a publication, please cite “C57BL/6JCya-Myo19em1flox/Cya mice (Catalog S-CKO-12937) were purchased from Cyagen.”
Strain Description
Ensembl Number
ENSMUST00000093969
NCBI RefSeq
NM_025414
Target Region
Exon 6
Size of Effective Region
~0.6 kb
Detailed Document
Overview of Gene Research
Myo19, a member of a novel class of myosin, is an actin-based motor that has a crucial role in mitochondrial homeostasis. It is associated with pathways related to mitochondrial dynamics, such as fission and fusion, and is important for maintaining mitochondrial function and cellular processes like cell division. Genetic models, especially knockout models, can be valuable for studying its functions [2,3,7].
In Myo19-deficient HEK293T cells, mitochondria were not properly fragmented during mitosis and were asymmetrically partitioned to daughter cells. Respiratory functions of mitochondria were impaired, ROS generation was enhanced, and cell proliferation, cytokinesis, and cell-matrix adhesion were negatively affected. Myo19 also regulates focal adhesions in interphase, and mitochondrial fusion and mitochondrially associated levels of fission protein Drp1 and adaptor proteins dynactin and TRAK1 at prometaphase [6].
Myo19 knockdown in other cell systems induced mitochondrial elongation, while overexpression induced fragmentation. This fragmentation was blocked by a Myo19 mutation predicted to inhibit ATPase activity and strong actin binding. Myo19-driven fragmentation was blocked by depletion of either the CAAX splice variant of the endoplasmic reticulum-anchored formin INF2 or the mitochondrially localized F-actin nucleator Spire1C, suggesting that Myo19 promotes fission by stabilizing mitochondria-ER contacts [1].
Loss of Myo19 in some studies enhanced the microenvironmental ROS gradient and chemotaxis, increasing tumor metastasis [4]. Also, depletion of Myo19 or disruption of its motor activity led to altered mitochondria membrane potential and decreased oxidative phosphorylation (OXPHOS), as it is critical for maintaining cristae structure by associating with the SAM-MICOS super complex [5].
In conclusion, Myo19 is essential for mitochondrial fission, proper mitochondrial partitioning during cell division, maintaining cristae structure for OXPHOS, and preventing enhanced tumor metastasis by regulating the microenvironmental ROS gradient. The use of Myo19-deficient models has significantly contributed to understanding its role in these biological processes and disease-related conditions, providing insights into potential therapeutic targets for diseases associated with mitochondrial dysfunction and cancer metastasis.
References:
1. Coscia, Stephen M, Thompson, Cameron P, Tang, Qing, Lakadamyali, Melike, Holzbaur, Erika L F. 2023. Myo19 tethers mitochondria to endoplasmic reticulum-associated actin to promote mitochondrial fission. In Journal of cell science, 136, . doi:10.1242/jcs.260612. https://pubmed.ncbi.nlm.nih.gov/36744380/
2. Bocanegra, Jennifer L, Adikes, Rebecca, Quintero, Omar A. . Myosin XIX. In Advances in experimental medicine and biology, 1239, 439-451. doi:10.1007/978-3-030-38062-5_20. https://pubmed.ncbi.nlm.nih.gov/32451871/
3. Shneyer, Boris I, Ušaj, Marko, Henn, Arnon. 2015. Myo19 is an outer mitochondrial membrane motor and effector of starvation-induced filopodia. In Journal of cell science, 129, 543-56. doi:10.1242/jcs.175349. https://pubmed.ncbi.nlm.nih.gov/26659663/
4. Ren, Xiaoyu, Shi, Peng, Su, Jing, Hu, Yiping, Wu, Congying. 2024. Loss of Myo19 increases metastasis by enhancing microenvironmental ROS gradient and chemotaxis. In EMBO reports, 25, 971-990. doi:10.1038/s44319-023-00052-y. https://pubmed.ncbi.nlm.nih.gov/38279020/
5. Shi, Peng, Ren, Xiaoyu, Meng, Jie, Li, Bo, Wu, Congying. 2022. Mechanical instability generated by Myosin 19 contributes to mitochondria cristae architecture and OXPHOS. In Nature communications, 13, 2673. doi:10.1038/s41467-022-30431-3. https://pubmed.ncbi.nlm.nih.gov/35562374/
6. Majstrowicz, Katarzyna, Honnert, Ulrike, Nikolaus, Petra, Hemkemeyer, Sandra A, Bähler, Martin. 2021. Coordination of mitochondrial and cellular dynamics by the actin-based motor Myo19. In Journal of cell science, 134, . doi:10.1242/jcs.255844. https://pubmed.ncbi.nlm.nih.gov/34013964/
7. Quintero, Omar A, DiVito, Melinda M, Adikes, Rebecca C, Feliu, Marianela, Cheney, Richard E. 2009. Human Myo19 is a novel myosin that associates with mitochondria. In Current biology : CB, 19, 2008-13. doi:10.1016/j.cub.2009.10.026. https://pubmed.ncbi.nlm.nih.gov/19932026/
Quality Control Standard
Sperm Test
Pre-cryopreservation: Measurement of sperm concentration, determination of sperm viability.
Post-cryopreservation: A vial of cryopreserved sperms is selected for in-vitro fertilization from each batch.
Environmental Standards:SPF
Available Region:Global
Source:Cyagen