WordNet

to put down by force or authority; "suppress a nascent uprising"; "stamp down on littering"; "conquer ones desires" (同)stamp down, inhibit, subdue, conquer, curb
reduce the incidence or severity of or stop; "suppress a yawn"; "this drug can suppress the hemorrhage"
put out of ones consciousness (同)repress
an electrical device for suppressing unwanted currents (同)suppresser
someone who suppresses; "dictators are suppressors of free speech" (同)suppresser
a gene that suppresses the phenotypic expression of another gene (especially of a mutant gene) (同)suppresser, suppressor_gene, suppresser gene
(genetics) any event that changes genetic structure; any alteration in the inherited nucleic acid sequence of the genotype of an organism (同)genetic mutation, chromosomal_mutation
a change or alteration in form or qualities

PrepTutorEJDIC

〈反乱など〉‘を'『鎮圧する』…,‘の'活動を押える / 〈感情・欲望など〉‘を'『抑制する』,抑える / …‘の'発表を禁止する,伏せる
抑圧する人,鎮圧者 / (ラジオ・テレビの)妨害電波(混信)防止装置
変化,俸転 / (生物の)突然変異;その変種

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/07/04 10:48:04」(JST)

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A suppressor mutation is a second mutation that alleviates or reverts the phenotypic effects of an already existing mutation. Genetic suppression therefore restores the phenotype seen prior to the original background mutation.^[1] Suppressor mutations are useful for identifying new genetic sites which affect a biological process of interest. They also provide evidence between functionally interacting molecules and intersecting biological pathways.^[2]

Intragenic vs. Intergenic Suppression

Intragenic Suppression

Intragenic suppression results from suppressor mutations that occur in the same gene as the original mutation. In a classic study, Francis Crick (et al.) used intragenic suppression to study the fundamental nature of the genetic code. From this study it was shown that genes are expressed as non-overlapping triplets (codons).^[1]

Researchers showed that mutations caused by either a single base insertion (+) or a single base deletion (-) could be “suppressed” or restored by a second mutation of the opposite sign, as long as the two mutations occurred in the same vicinity of the gene. This led to the conclusion that genes needed to be read in a specific “reading frame” and a single base insertion or deletion would shift the reading frame (frameshift mutation) in such a way that the remaining DNA would code for a different polypeptide than the one intended. Therefore, researchers concluded that the second mutation of opposite sign suppresses the original mutation by restoring the reading frame, as long as the portion between the two mutations is not critical for protein function.^[1]

In addition to the reading frame, Crick also used suppressor mutations to determine codon size. It was found that while one and two base insertions/deletions of the same sign resulted in a mutant phenotype, deleting or inserting three bases could give a wild type phenotype. From these results it was concluded that an inserted or deleted triplet does not disturb the reading frame and the genetic code is in fact a triplet.^[1]

Intergenic Suppression

Intergenic (also known as extragenic) suppression relieves the effects of a mutation in one gene by a mutation somewhere else within the genome. The second mutation is not on the same gene as the original mutation.^[2] Intergenic suppression is useful for identifying and studying interactions between molecules, such as proteins. For example, a mutation which disrupts the complementary interaction between protein molecules may be compensated for by a second mutation elsewhere in the genome that restores or provides a suitable alternative interaction between those molecules. Several proteins of biochemical, signal transduction, and gene expression pathways have been identified using this approach. Examples of such pathways include receptor-ligand interactions as well as the interaction of components involved in DNA replication, transcription, and translation.^[1]

References

^ ^a ^b ^c ^d ^e Hartwell, L. H., Hood, L., Goldberg, M. L., Reynolds, A. E., Silver, L. M., & Veres, R. C. (2008). Genetics: From Genes to Genomes. New York: McGraw-Hill.
^ ^a ^b Hodgkin J. Genetic suppression. 2005 Dec 27. In: WormBook: The Online Review of C. elegans Biology [Internet]. Pasadena (CA): WormBook; 2005-.

External links

The mutations chapter of the WikiBooks General Biology textbook
Examples of Beneficial Mutations

UpToDate Contents

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1. 大腸癌の分子遺伝学 molecular genetics of colorectal cancer
2. 急性骨髄性白血病の分子遺伝学 molecular genetics of acute myeloid leukemia
3. 軟部および骨肉腫の病原因子 pathogenetic factors in soft tissue and bone sarcomas
4. カウデン症候群などのPTEN過誤腫症候群 pten hamartoma tumor syndrome including cowden syndrome
5. 前立腺癌の分子生物学 molecular biology of prostate cancer

English Journal

Somatic alterations in juvenile polyps from BMPR1A and SMAD4 mutation carriers.

Blatter RH1, Plasilova M1,2, Wenzel F3, Gokaslan ST4, Terracciano L5, Ashfaq R6, Heinimann K1,3.
Genes, chromosomes & cancer.Genes Chromosomes Cancer.2015 Sep;54(9):575-82. doi: 10.1002/gcc.22270. Epub 2015 Jul 14.
Juvenile polyposis syndrome (JPS) is a rare autosomal dominant disorder predisposing to gastrointestinal hamartomatous polyps and cancer with a pathogenic SMAD4 or BMPR1A germline mutation (1st-hit) being identified in about 40-50% of patients. Little is known, however, about the occurrence and natu
PMID 26171675

Environmental disruption of circadian rhythm predisposes mice to osteoarthritis-like changes in knee joint.

Kc R1, Li X1, Voigt RM2, Ellman MB1,3, Summa KC4, Vitaterna MH4, Keshavarizian A2,5,6,7, Turek FW4, Meng QJ8, Stein GS9, van Wijnen AJ10, Chen D1, Forsyth CB2, Im HJ1,3,11,12,13.
Journal of cellular physiology.J Cell Physiol.2015 Sep;230(9):2174-83. doi: 10.1002/jcp.24946.
Circadian rhythm dysfunction is linked to many diseases, yet pathophysiological roles in articular cartilage homeostasis and degenerative joint disease including osteoarthritis (OA) remains to be investigated in vivo. Here, we tested whether environmental or genetic disruption of circadian homeostas
PMID 25655021

Immunohistochemical, genetic and clinical characterization of sporadic aldosterone-producing adenomas.

Monticone S1, Castellano I2, Versace K3, Lucatello B4, Veglio F5, Gomez-Sanchez CE6, Williams TA5, Mulatero P7.
Molecular and cellular endocrinology.Mol Cell Endocrinol.2015 Aug 15;411:146-54. doi: 10.1016/j.mce.2015.04.022. Epub 2015 May 6.
Adrenal glands removed for unilateral primary aldosteronism (PA) display marked histological heterogeneity. Recently reported somatic mutations in KCNJ5, ATP1A1, ATP2B3 and CACNA1D can partially account for these differences. In this study we aimed at combining phenotypic and genotypic characteristi
PMID 25958045

Japanese Journal

予後不良な経過をたどったBRAF遺伝子変異を伴うStage Ⅳ大腸癌の１例

稲田涼,永坂岳司,竹原清人,杉原正大,母里淑子,楳田祐三,久保田暢人,森川達也,近藤喜太,宇野太,貞森裕,八木孝仁,藤原俊義
岡山医学会雑誌 125(1), 47-50, 2013-04-01
… We performed an ileocecal resection, and the specimen showed poorly differentiated adenocarcinoma with mutation in the BRAF oncogene. … Multiple genetic and epigenetic alterations in oncogenes and tumor suppressor genes are involved in the process of colorectal carcinogenesis. … A mutation in the BRAF oncogene was reported to be associated with a very unfavorable prognosis in colorectal cancers. …
NAID 120005232683

Effects on vesicular transport pathways at the late endosome in cells with limited very long-chain fatty acids

Obara Keisuke,Kojima Ryo,Kihara Akio
Journal of Lipid Research 54(3), 831-842, 2013-03-00
… In the presented study, we screened for multicopy suppressors that rescued temperature-sensitive growth of VLCFA-limited yeast cells, and identified the VPS21 gene, encoding a Rab GTPase, as such a suppressor. … When the vps21Δ mutation was introduced into a deletion mutant of the SUR4 gene, which encodes a VLCFA elongase, a synthetic growth defect was observed. …
NAID 120005228358

Rabring7 Degrades c-Myc through Complex Formation with MM-1

Narita Rina,Kitaura Hirotake,Torii Ayako,Tashiro Erika,Miyazawa Makoto,Ariga Hiroyoshi,Iguchi-Ariga Sanae M. M.
PLoS One 7(7), e41891, 2012-07-23
… We have reported that a novel c-Myc-binding protein, MM-1, repressed E-box-dependent transcription and transforming activities of c-Myc and that a mutation of A157R in MM-1, which is often observed in patients with leukemia or lymphoma, abrogated all of the repressive activities of MM-1 toward c-Myc, indicating that MM-1 is a novel tumor suppressor. …
NAID 120004689030