Alternative titles; symbols
HGNC Approved Gene Symbol: MOS
Cytogenetic location: 8q12.1 Genomic coordinates (GRCh38): 8:56,112,942-56,113,982 (from NCBI)
| Location | Phenotype |
Phenotype MIM number |
Inheritance |
Phenotype mapping key |
|---|---|---|---|---|
| 8q12.1 | Oocyte/zygote/embryo maturation arrest 20 | 620383 | Autosomal recessive | 3 |
MOS is a serine/threonine kinase that activates the MAP kinase cascade through direct phosphorylation of the MAP kinase activator MEK (MAP2K1; 176872) (Prasad et al., 2008).
The Moloney murine sarcoma virus (MSV) is a representative of a class of replication-defective retroviruses that transform fibroblasts in culture and induce sarcomas in vivo. It arose by recombination between the Moloney murine leukemia virus and a sequence derived from mouse cells. The mouse cell-derived segment of MSV, termed v-mos, is required for induction and maintenance of viral transformation, and the normal mouse analog of v-mos has been cloned (Prakash et al., 1982).
By screening a placenta DNA library for homologs of mouse Mos, Watson et al. (1982) cloned human MOS. The deduced 346-amino acid human protein shares significant homology with the mouse protein, with regions of lowest homology near the N and C termini and in a central 11-amino acid stretch.
Using an S1 nuclease assay, Propst and Vande Woude (1985) detected Mos expression predominantly in mouse testis, ovary, and embryos. Northern blot analysis revealed a 1.7-kb transcript in testis and a 1.4-kb transcript in ovary. At least 2 major transcripts of 2.3 and 1.3 kb were detected in embryo RNA.
Using qualitative and semiquantitative RT-PCR of human and cynomolgus monkey oocytes, granulosa cells, and ovarian tissue, Heikinheimo et al. (1995) found that MOS was expressed in an oocyte-specific manner. No MOS expression was detected in granulosa cells. MOS mRNA was detected in human pre-embryos, but very little was detected in human embryos beyond the 6-cell stage, suggesting that the mRNA was of maternal origin and was degraded.
By analysis of reported RNA-seq data of human oocytes and early embryos, Zhang et al. (2021) found that MOS mRNA was highly expressed in oocytes but expression decreased markedly after fertilization, then slightly increased in 4-cell stage embryos, followed by a gradual decrease from 8-cell to blastocyst embryos.
Zeng et al. (2022) measured mRNA expression patterns of MOS using RT-PCR and found that MOS was highly expressed in human oocytes, including the germinal vesicle, metaphase I, and metaphase II stages, but was poorly expressed in early embryos and other somatic tissues.
Because of the evolutionary conservation of viral oncogenes among vertebrate species, Prakash et al. (1982) used the cloned mouse Mos analog to map the human MOS gene to chromosome 8.
By in situ hybridization, Neel et al. (1982) assigned the MOS gene to chromosome 8q22. They used the method of Kirsch et al. (1982).
Rowley (1973, 1983) located the MOS oncogene at the chromosome 8 breakpoint of the 8;21 translocation associated with acute myeloblastic leukemia.
Caubet et al. (1985) studied the regional assignment of MOS by in situ hybridization and by hybridization to flow-sorted chromosomes from a cell line with a translocation t(6;8)(q27;q21). Both approaches yielded results indicating 8q11 as the site of MOS, not 8q22 as previously reported. By in situ hybridization, Testa et al. (1988) likewise assigned the MOS gene to chromosome 8q11-q12.
By in situ hybridization to metaphase chromosomes and by standard genetic backcrosses, Propst et al. (1989) demonstrated that Mos maps near the centromere of mouse chromosome 4. It had previously been assigned to mouse chromosome 4 by use of panels of mouse/hamster somatic cell hybrids (Swan et al., 1982). Dandoy et al. (1989) showed by linkage analysis that the murine Mos gene is located in the region of chromosome 4 compatible with the physical mapping (Threadgill and Womack, 1988) by in situ hybridization.
Lenormand et al. (1997) stated that overexpression of rat Mos in the C2C12 mouse myoblast cell line activated muscle differentiation, whereas inhibition of endogenous Mos via antisense RNA caused reversible blockage of myogenesis. They found that constitutive Mos expression in C2C12 myoblasts activated Myod (MYOD1; 159970) expression as well as myogenesis. Transient transfection assays showed that Mos bound unphosphorylated Myod and enhanced the ability of Myod to activate target muscle enhancers. Phosphorylation of recombinant Myod by Mos inhibited the DNA-binding activity of Myod homodimers and promoted the formation and DNA-binding activity of Myod-E12 (TCF3; 147141) heterodimers. Lenormand et al. (1997) concluded that interaction with and phosphorylation of MYOD by MOS enhances muscle differentiation.
Full-grown Xenopus oocytes arrest at the G2/M border of meiosis I. Progesterone breaks this arrest, leading to resumption of the meiotic cell cycles and maturation of the oocyte into a fertilizable egg. In these oocytes, progesterone interacts with an unidentified surface-associated receptor, which induces a nontranscriptional signaling pathway that stimulates the translation of dormant c-mos mRNA. Translational recruitment of c-mos and several other mRNAs is regulated by cytoplasmic polyadenylation, a process that requires two 3-prime untranslated regions, the cytoplasmic polyadenylation element (CPE) and the polyadenylation hexanucleotide AAUAAA. Mendez et al. (2000) demonstrated that early site-specific phosphorylation of CPEB (CPEB1; 607342), which was catalyzed by Eg2 (see 603495), was essential for polyadenylation of c-mos mRNA, subsequent translation of c-mos, and oocyte maturation.
Prasad et al. (2008) noted that the temporal requirements for MOS function differ between mammalian oocytes and Xenopus oocytes. MOS is required for meiotic metaphase II arrest in both mammalian and Xenopus oocytes; however, Mos is also required earlier during maturation of Xenopus oocytes, but not mammalian oocytes, to mediate the meiosis I and meiosis II transition. Prasad et al. (2008) found that, similar to Xenopus Mos, a CPE in the 3-prime UTR of the human MOS transcript was bound by CPEB1 and directed maturation-dependent cytoplasmic polyadenylation in human oocytes. The 3-prime UTR of Xenopus Mos also contains a polyadenylation response element (PRE) that is bound by Musashi (see MSI1; 603328) and directs early polyadenylation during progesterone-stimulated oocyte maturation. Prasad et al. (2008) found that this PRE was absent in the 3-prime UTRs of rat, mouse, monkey, and human MOS. They concluded that species-specific differences in 3-prime UTR regulatory element composition contribute to the differential temporal activation of MOS mRNA translation during Xenopus and mammalian oocyte maturation.
Zhang et al. (2021) studied Mos-deficient mouse oocytes and observed that F-actin signal was much weakened compared to wildtype oocytes. Inactivation of ERK1 (MAPK3; 601795)/ERK2 (MAPK1: 176948) resulted in reduced cortical F-actin in both mouse and human oocytes. In addition, Mos knockdown or ERK1/2 inactivation caused alpha-tubulin (see 602529) instability. The authors concluded that the MOS-mediated ERK1/2 signaling pathway is essential for oocyte cytoskeleton homeostasis. In addition, analysis of RNA sequencing data revealed that MOS mutations or ERK1/2 inhibition in human mature oocytes prevented the decrease in transcripts that normally occurs during the transition from the germinal vesicle stage to metaphase II, suggesting that the MOS-ERK signaling cascade governs maternal mRNA clearance during human oocyte maturation. The authors also found that the human MOS-ERK cascade is required for maintaining mitochondrial function through accelerating mitochondrial mRNA clearance during oocyte maturation.
A nonrandom chromosome translocation, t(8;21)(q22;q22), which results in an 8q- and 21q+ chromosome, is seen almost exclusively in the M2 subtype of acute myeloblastic leukemia (AML with maturation). Band 21q22 is critical to the Down syndrome (190685) phenotype, which is associated with an increased leukemia risk. In studies of a case of AML-M2, Drabkin et al. (1985) isolated the 21q+ chromosome in a somatic cell hybrid and showed that the MOS oncogene had not been translocated to chromosome 21. They also could find no rearrangement in a 12.4-kb region surrounding the MOS gene.
In 3 unrelated Han Chinese women with infertility due to early embryonic arrest and fragmentation (OZEMA20; 620383), Zhang et al. (2021) identified biallelic mutations in the MOS gene: homozygosity for a missense mutation (N95K; 190060.0001) in 1 patient, compound heterozygosity for 2 missense mutations, M139T (190060.0002) and R246H (190060.0003), in the second patient, and homozygosity for a nonsense mutation (C320X; 190060.0004) in the third patient. The mutations segregated fully with disease in each of the families and were not found in fertile controls; only the N95K substitution was present in public variant databases, at low minor allele frequency. The mutants showed reduced activation of downstream targets and attenuated rescue of the Mos-knockdown phenotype in mouse oocytes compared to wildtype MOS.
By WES in 2 unrelated Chinese women with infertility due to preimplantation embryonic arrest, Zeng et al. (2022) identified biallelic mutations in the MOS gene: the first was homozygous for the previously reported N95K variant, and the second was compound heterozygous for a 1-bp deletion (190060.0005) and an R319H substitution (190060.0006), for which her parents were heterozygous carriers. All 3 mutants showed reduced phosphorylation of the MOS downstream targets ERK1/2 compared to wildtype MOS.
By WES in 3 Chinese women with infertility due to extrusion of a large polar body 1 (PB1) and early embryonic arrest, who were negative for mutation in the TUBB8 (616768) or PATL2 (617743) genes, Zhang et al. (2022) identified biallelic missense mutations in the MOS gene, including homozygosity for a S264C substitution (190060.0007) in patient 1 and compound heterozygosity for H199L (190060.0008) and A229V (190060.0009) in the twin sisters (patients 2 and 3). The mutations were not found in 100 fertile Chinese women or in public variant databases, and the mutant proteins showed reduced activation of downstream targets compared to wildtype MOS and could not rescue symmetric division of oocytes in Mos-knockdown cells.
In a 25-year-old Chinese woman with infertility due to extrusion of a large PB1 with embryonic arrest and fragmentation, Jiao et al. (2022) identified homozygosity for a missense mutation in the MOS gene (I197M; 190060.0010). The mutation segregated with disease and was not found in public variant databases.
Hashimoto et al. (1994) found that Mos -/- mice appeared normal and grew at the same rate as wildtype mice. Reproduction was normal in male Mos -/- mice, but Mos -/- females exhibited very low fertility and developed ovarian teratomas at a high frequency. In Mos -/- ovaries, many oocytes were activated and showed nuclear formation and cell division, indicating that Mos -/- oocytes were activated parthenogenetically before or just after ovulation. In vitro, most Mos -/- oocytes lost the capacity for penetration by sperm. Hashimoto et al. (1994) concluded that, in contrast to the role of Mos in several steps of Xenopus oocyte maturation, mouse Mos acts almost exclusively in the second meiotic metaphase arrest and is an essential component of the cytostatic factor.
In a 40-year-old Han Chinese woman (family 1) with infertility due to early embryonic arrest and fragmentation (OZEMA20; 620383), Zhang et al. (2021) identified homozygosity for a c.285C-A transversion (c.285C-A, NM_005372.1) in the MOS gene, resulting in an asn95-to-lys (N95K) substitution at a highly conserved residue within the protein kinase domain. Her consanguineous parents were heterozygous for the mutation, which was not found in 100 fertile controls, but was present in the ExAC and gnomAD databases, at low minor allele frequency (0.0000329 and 0.0000163, respectively). Because MOS mediates phosphorylation of MEK1 (MAP2K1; 176872)/MEK2 (MAP2K2; 601263), resulting in activation of ERK1 (MAPK3; 601795)/ERK2 (MAPK1: 176948) during oocyte maturation, the authors analyzed ERK1/ERK2 phosphorylation and found significantly reduced activation levels in patient oocytes compared to controls. Overexpression of the N95K variant in HEK293 cells did not effectively activate MEK1/2 or ERK1/2, whereas wildtype MOS remarkably enhanced phosphorylation. Coimmunoprecipitation studies showed that the N95K mutant had weaker interaction with MEK1 than wildtype MOS. In mouse oocytes, immunofluorescent staining and Western blot showed significantly lower phosphorylation of ERK1/2 with the N95K mutant compared to wildtype MOS. The mutant protein also showed attenuated rescue of cortical F-actin assembly in mouse oocytes compared to wildtype MOS. Analysis of RNA sequencing data in patient oocytes compared to controls revealed that the N95K mutation prevented the decrease in transcripts that normally occurs during the transition from the germinal vesicle stage to metaphase II, suggesting that the MOS-ERK signaling cascade governs maternal mRNA clearance during human oocyte maturation.
In a 34-year-old Chinese woman (patient 1) with infertility due to preimplantation embryonic arrest, Zeng et al. (2022) identified homozygosity for the previously reported N95K substitution in the MOS gene. Analysis of transfected HEK293T cells showed that the N95K mutation significantly decreased the protein expression level, and there was significantly reduced activation of the MOS downstream targets ERK1/2 with the mutant compared to wildtype. In addition, compared to wildtype MOS, the N95K mutant exhibited significantly reduced ability to rescue the Mos-knockdown phenotype in mouse oocytes (loss of maintenance of metaphase II arrest and absence of cortical F-actin thickening).
In a 31-year-old Han Chinese woman (patient 2) with infertility due to early embryonic arrest and fragmentation (OZEMA20; 620383), Zhang et al. (2021) identified compound heterozygosity for missense mutations in the MOS gene: a c.416T-C transition (c.416T-C, NM_005372.1), resulting in a met139-to-thr (M139T) substitution, and a c.737G-A transition, resulting in an arg246-to-his (R246H; 190060.0003) substitution. Both substitutions occurred at highly conserved residues within the protein kinase domain. Her parents were each heterozygous for 1 of the mutations, neither of which was found in 100 fertile controls or in the ExAC or gnomAD databases. Overexpression of the combined M139T/R246H variants in HEK293 cells did not effectively activate MEK1 (MAP2K1; 176872)/MEK2 (MAP2K2; 601263) or ERK1 (MAPK3; 601795)/ERK2 (MAPK1: 176948), whereas wildtype MOS remarkably enhanced phosphorylation. Coimmunoprecipitation studies showed that the R246H mutant had weaker interaction with MEK1 than wildtype MOS. In mouse oocytes, immunofluorescent staining and Western blot showed lower phosphorylation of ERK1/2 with the combined M139T/R246H mutant compared to wildtype MOS. The combined mutant proteins also showed attenuated rescue of cortical F-actin assembly in mouse oocytes compared to wildtype MOS.
For discussion of the c.737G-A transition (c.737G-A, NM_005372.1) in the MOS gene, resulting in an arg246-to-his (R246H) substitution, that was found in compound heterozygous state in a 31-year-old Han Chinese woman (patient 2) with infertility due to early embryonic arrest and fragmentation (OZEMA20; 620383) by Zhang et al. (2021), see 190060.0002.
In a 34-year-old Han Chinese woman (patient 3) with infertility due to early embryonic arrest and fragmentation (OZEMA20; 620383), Zhang et al. (2021) identified homozygosity for a c.960C-A transversion (c.960C-A, NM_005372.1) in the MOS gene, resulting in a cys320-to-ter (C320X) substitution at a highly conserved residue within the protein kinase domain. Her consanguineous parents were heterozygous for the mutation, which was not found in 100 fertile controls or in the ExAC or gnomAD databases. Overexpression of the C320X variant in HEK293 cells did not effectively activate MEK1 (MAP2K1; 176872)/MEK2 (MAP2K2; 601263) or ERK1 (MAPK3; 601795)/ERK2 (MAPK1; 176948), whereas wildtype MOS remarkably enhanced phosphorylation. Coimmunoprecipitation studies showed that the C320X mutant had minimal interaction with MEK1 compared to wildtype MOS. In mouse oocytes, immunofluorescent staining showed significantly lower phosphorylation of ERK1/2, and Western blot showed almost complete inactivation of ERK1/2, with the C320X mutant compared to wildtype MOS. The mutant protein also showed attenuated rescue of cortical F-actin assembly in mouse oocytes compared to wildtype MOS.
In a 31-year-old Chinese woman (patient 2) with infertility due to preimplantation embryonic arrest (OZEMA20; 620383), Zeng et al. (2022) identified compound heterozygosity for a 1-bp deletion (c.467delG, NM_005372.1) in the MOS gene, causing a frameshift resulting in a premature termination codon (Gly156AlafsTer18), and a c.956G-A transition, resulting in an arg319-to-his (R319H; 190060.0006) substitution at a conserved residue within the protein kinase domain. Analysis of transfected HEK293T cells showed severely reduced protein quantity with the truncating mutation, and significantly reduced activation of the MOS downstream targets ERK1 (MAPK3; 601795)/ERK2 (MAPK1; 176948) with either mutant compared to wildtype. In addition, compared to wildtype MOS, both mutants exhibited a significantly reduced ability to rescue the Mos-knockdown phenotype in mouse oocytes (loss of maintenance of metaphase II arrest and absence of cortical F-actin thickening).
For discussion of the c.956G-A transition (c.956G-A, NM_005372.1) in the MOS gene, resulting in an arg319-to-his (R319H) substitution, that was found in compound heterozygous state in a 31-year-old Chinese woman (patient 2) with infertility due to preimplantation embryonic arrest (OZEMA20; 620383) by Zeng et al. (2022), see 190060.0005.
In a 29-year-old Chinese woman (patient 1) with infertility due to extrusion of a large polar body 1 and early embryonic arrest (OZEMA20; 620383), Zhang et al. (2022) identified homozygosity for a c.791C-G transversion (c.791C-G, NM_005372.1) in the MOS gene, resulting in a ser264-to-cys (S264C) substitution at a highly conserved residue within the protein kinase domain. DNA from her consanguineous parents was unavailable for segregation analysis, but the S264C variant was not found in 100 fertile Chinese women or in the ExAC or gnomAD databases. Analysis of transfected HEK293 cells showed a significantly reduced level of S264C protein, and the S264C mutant completely failed to activate the MOS downstream targets ERK1 (MAPK3; 601795)/ERK2 (MAPK1; 176948). Coimmunoprecipitation studies showed that the S264C mutant displayed decreased interaction with MEK1 (MAP2K1; 176872) compared to wildtype MOS. In addition, the S264C mutant could not rescue symmetric division of mouse oocytes after siRNA knockdown (siMos).
In 28-year-old Chinese twin sisters (patients 2 and 3) with infertility due to extrusion of a large polar body 1 and early embryonic arrest (OZEMA20; 620383), Zhang et al. (2022) identified compound heterozygosity for a c.596A-T transversion (c.596A-T, NM_005372.1) in the MOS gene, resulting in a his199-to-leu (H199L) substitution, and a c.875C-T transition, resulting in an ala229-to-val (A229V; 190060.0009) substitution. Both substitutions occur at highly conserved residues within the protein kinase domain. Their parents were each heterozygous for 1 of the mutations, which were not found in 100 fertile Chinese women or in the ExAC or gnomAD databases. Analysis of transfected HEK293 cells showed a significantly reduced level of H199L protein, whereas A229V levels were comparable to wildtype, and the H199L mutant completely failed to activate the MOS downstream targets ERK1 (MAPK3; 601795)/ERK2 (MAPK1; 176948), whereas the A229V mutant showed reduced ERK1/2 activation. Coimmunoprecipitation studies showed that both mutants displayed decreased interaction with MEK1 (MAP2K1; 176872) compared to wildtype MOS. In addition, the combined H199L/A229V mutants could not rescue symmetric division of mouse oocytes after siMos knockdown.
For discussion of the c.875C-T transition (c.875C-T, NM_005372.1) in the MOS gene, resulting in an ala229-to-val (A229V) substitution, that was found in compound heterozygous state in 28-year-old Chinese twin sisters (patients 2 and 3) with infertility due to extrusion of a large polar body 1 and early embryonic arrest (OZEMA20; 620383) by Zhang et al. (2022), see 190060.0008.
In a 25-year-old Chinese woman with infertility due to extrusion of a large polar body 1 and embryonic arrest with fragmentation (OZEMA20; 620383), Jiao et al. (2022) identified homozygosity for a c.591T-G transversion (c.591T-G, NM_005372.1) in the MOS gene, resulting in an ile197-to-met (I197M) substitution at a highly conserved residue. Her unaffected parents were heterozygous for the mutation, which was not found in the 1000 Genomes Project or gnomAD databases.
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Zhang, Y.-L., Zheng, W., Ren, P., Hu, H., Tong, X., Zhang, S.-P., Li, X., Wang, H., Jiang, J.-C., Jin, J., Yang, W., Cao, L., and 11 others. Biallelic mutations in MOS cause female infertility characterized by human early embryonic arrest and fragmentation. EMBO Molec. Med. 13: e14887, 2021. [PubMed: 34779126] [Full Text: https://doi.org/10.15252/emmm.202114887]
Zhang, Y.-L., Zheng, W., Ren, P., Jin, J., Hu, Z., Liu, Q., Fan, H.-Y., Gong, F., Lu, G.-X., Lin, G., Zhang, S., Tong, X. Biallelic variants in MOS cause large polar body in oocyte and human female infertility. Hum. Reprod. 37: 1932-1944, 2022. [PubMed: 35670744] [Full Text: https://doi.org/10.1093/humrep/deac120]