Knowledge (XXG)

Anticipation (genetics)

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in DNA occurs. All of these diseases have neurological symptoms. Prior to the understanding of the genetic mechanism for anticipation, it was debated whether anticipation was a true biological phenomenon or whether the earlier age of diagnosis was related to heightened awareness of disease symptoms
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that increases the number of repeats in offspring inheriting the mutant allele. Once the number of copies reaches over 100, the disease will manifest earlier in life (although the individual will still reach adulthood before the symptoms are evident) and the symptoms will be more severe – including
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For many of the loci, trinucleotide expansion is harmless, but in some areas expansion has detrimental effects that cause symptoms. When the trinucleotide repeat is present within the protein-coding region, the repeat expansion leads to production of a mutant protein with
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In order to have a deleterious effect, the number of repeats must cross a certain threshold. For example, normal individuals have between 5 and 30 CTG repeats within the 3' UTR of
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The mechanism behind the expansion of the triplet repeats is not well understood. One hypothesis is that the increasing number of repeats influences the overall shape of the
319: 152:. If the number of repeats is between 50 and 100, the person is only mildly affected – perhaps having only cataracts. However, meiotic instability could result in a 260:
Armanios M., Chen J. L., Chang Y. P., Brodsky R. A., Hawkins A., Griffin C. A., Eshleman J. R., Cohen A. R., Chakravarti A., Hamosh A., Greider C. W. (2005).
471: 121:, where the trinucleotide repeat encodes a long stretch of glutamine residues. When the repeat is present in an untranslated region, it could affect the 645: 464: 516: 546: 508: 74: 33: 262:"Haploinsufficiency of telomerase reverse transcriptase leads to anticipation in autosomal dominant dyskeratosis congenita" 499: 212:– GAA (Note: Friedreich ataxia does not usually exhibit anticipation because it is an autosomal recessive disorder.) 487: 450: 521: 184: 179: 118: 37: 623: 583: 576: 562: 535: 531: 196: 238: 313: 161:. As the number progresses upwards past 400, the symptoms show themselves during childhood or infancy. 24:
is a phenomenon whereby as a genetic disorder is passed on to the next generation, the symptoms of the
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Polito, J.M.; Mendeloff, A.I; Harris, M.L; Bayless, T.M; Childs, Barton; Rees, R.C (23 March 1996).
32:. In most cases, an increase in the severity of symptoms is also noted. Anticipation is common in 204: 605: 569: 555: 376: 222: 190: 173: 149: 138: 41: 446: 233: 425: 368: 301: 209: 134: 415: 407: 358: 291: 281: 153: 58: 45: 25: 456: 122: 277: 89:, unstable repeats can undergo triplet expansion (see later section); in this case, the 420: 395: 296: 261: 101: 363: 346: 639: 380: 62: 93:
produced have a greater number of repeats than are found in the somatic tissues.
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Fresko, I; M Soy; V Hamuryudan; S Yurdakul; Ş Yavuz; Z Tümerd; H Yazici (1998).
82: 332: 90: 29: 286: 130: 305: 78: 429: 372: 217: 158: 114: 17: 411: 86: 66: 347:"Preliminary evidence for genetic anticipation in Crohn's disease" 70: 126: 460: 97: 85:(e.g. CGG) which is repeated a number of times. During 615: 597: 545: 507: 498: 100:, which can have an effect on its interaction with 57:Trinucleotide repeats are apparent in a number of 472: 8: 318:: CS1 maint: multiple names: authors list ( 28:become apparent at an earlier age with each 396:"Genetic anticipation in Behçet's syndrome" 504: 479: 465: 457: 449:at the U.S. National Library of Medicine 419: 362: 295: 285: 165:Examples of diseases showing anticipation 532:Spinocerebellar ataxia 1, 2, 3, 6, 7, 17 252: 169:Diseases showing anticipation include: 81:'s. They consist of a pattern of three 311: 104:and thus the expression of the gene. 7: 517:Dentatorubral-pallidoluysian atrophy 335:, NCBI Bookshelf: Friedreich Ataxia. 199:– TTAGGG (telomere repeat sequence) 53:Trinucleotide repeats and expansion 129:in which the repeat is found (ex. 14: 646:Genetic disorders by mechanism 148:, the gene that is altered in 34:trinucleotide repeat disorders 1: 364:10.1016/S0140-6736(96)90870-3 662: 509:Polyglutamine (PolyQ), CAG 133:) or many genes through a 65:. They have been found in 624:Spinocerebellar ataxia 10 606:Myotonic dystrophy type 2 584:Spinocerebellar ataxia 12 570:Myotonic dystrophy type 1 488:Non-Mendelian inheritance 577:Spinocerebellar ataxia 8 451:Medical Subject Headings 266:Proc Natl Acad Sci U S A 230:Without expression type 117:. This is the case for 287:10.1073/pnas.0508124102 180:spinocerebellar ataxias 536:Machado-Joseph disease 197:Dyskeratosis congenita 522:Huntington's disease 447:Genetic+anticipation 185:Huntington's disease 119:Huntington's disease 38:Huntington's disease 563:Friedreich's ataxia 412:10.1136/ard.57.1.45 278:2005PNAS..10215960A 205:Autosomal recessive 556:Fragile X syndrome 223:Fragile X syndrome 191:Myotonic dystrophy 174:Autosomal dominant 150:myotonic dystrophy 139:myotonic dystrophy 108:Disease mechanisms 42:myotonic dystrophy 633: 632: 593: 592: 547:Non-polyglutamine 357:(9004): 798–800. 210:Friedreich ataxia 135:dominant negative 49:within a family. 653: 505: 481: 474: 467: 458: 434: 433: 423: 391: 385: 384: 366: 342: 336: 330: 324: 323: 317: 309: 299: 289: 257: 239:Behçet's disease 154:dynamic mutation 115:gain of function 46:dynamic mutation 26:genetic disorder 661: 660: 656: 655: 654: 652: 651: 650: 636: 635: 634: 629: 616:Pentanucleotide 611: 598:Tetranucleotide 589: 541: 527:Kennedy disease 494: 485: 443: 438: 437: 393: 392: 388: 344: 343: 339: 331: 327: 310: 272:(44): 15960–4. 259: 258: 254: 249: 234:Crohn's disease 167: 110: 55: 12: 11: 5: 659: 657: 649: 648: 638: 637: 631: 630: 628: 627: 619: 617: 613: 612: 610: 609: 601: 599: 595: 594: 591: 590: 588: 587: 580: 573: 566: 559: 551: 549: 543: 542: 540: 539: 529: 524: 519: 513: 511: 502: 496: 495: 486: 484: 483: 476: 469: 461: 455: 454: 442: 441:External links 439: 436: 435: 386: 337: 325: 251: 250: 248: 245: 244: 243: 242: 241: 236: 228: 227: 226: 215: 214: 213: 202: 201: 200: 194: 188: 182: 166: 163: 109: 106: 102:DNA polymerase 54: 51: 13: 10: 9: 6: 4: 3: 2: 658: 647: 644: 643: 641: 625: 621: 620: 618: 614: 607: 603: 602: 600: 596: 585: 581: 578: 574: 571: 567: 564: 560: 557: 553: 552: 550: 548: 544: 537: 533: 530: 528: 525: 523: 520: 518: 515: 514: 512: 510: 506: 503: 501: 500:Trinucleotide 497: 493: 489: 482: 477: 475: 470: 468: 463: 462: 459: 452: 448: 445: 444: 440: 431: 427: 422: 417: 413: 409: 405: 401: 400:Ann Rheum Dis 397: 390: 387: 382: 378: 374: 370: 365: 360: 356: 352: 348: 341: 338: 334: 329: 326: 321: 315: 307: 303: 298: 293: 288: 283: 279: 275: 271: 267: 263: 256: 253: 246: 240: 237: 235: 232: 231: 229: 224: 221: 220: 219: 216: 211: 208: 207: 206: 203: 198: 195: 192: 189: 186: 183: 181: 177: 176: 175: 172: 171: 170: 164: 162: 160: 155: 151: 147: 142: 140: 136: 132: 128: 124: 120: 116: 107: 105: 103: 99: 94: 92: 88: 84: 80: 76: 72: 68: 64: 60: 52: 50: 47: 43: 39: 35: 31: 27: 23: 19: 492:anticipation 491: 406:(1): 45–48. 403: 399: 389: 354: 350: 340: 328: 314:cite journal 269: 265: 255: 168: 145: 143: 137:effect (ex. 111: 95: 63:human genome 56: 22:anticipation 21: 15: 157:electrical 83:nucleotides 351:The Lancet 247:References 123:expression 91:germ cells 44:, where a 36:, such as 30:generation 333:Link text 131:fragile X 640:Category 381:21921598 306:16247010 218:X-linked 178:Several 159:myotonia 18:genetics 622:ATTCT ( 430:9536823 421:1752455 373:8622336 297:1276104 274:Bibcode 125:of the 87:meiosis 67:introns 61:in the 604:CCTG ( 453:(MeSH) 428:  418:  379:  371:  304:  294:  79:3' UTR 582:CAG ( 575:CTG ( 568:CTG ( 561:GAA ( 554:CGG ( 377:S2CID 225:– CGG 193:– CTG 187:– CAG 71:exons 426:PMID 369:PMID 320:link 302:PMID 146:DMPK 127:gene 73:and 59:loci 40:and 416:PMC 408:doi 359:doi 355:347 292:PMC 282:doi 270:102 141:). 98:DNA 77:or 16:In 642:: 490:: 424:. 414:. 404:57 402:. 398:. 375:. 367:. 353:. 349:. 316:}} 312:{{ 300:. 290:. 280:. 268:. 264:. 75:5' 69:, 20:, 626:) 608:) 586:) 579:) 572:) 565:) 558:) 538:) 534:( 480:e 473:t 466:v 432:. 410:: 383:. 361:: 322:) 308:. 284:: 276::

Index

genetics
genetic disorder
generation
trinucleotide repeat disorders
Huntington's disease
myotonic dystrophy
dynamic mutation
loci
human genome
introns
exons
5'
3' UTR
nucleotides
meiosis
germ cells
DNA
DNA polymerase
gain of function
Huntington's disease
expression
gene
fragile X
dominant negative
myotonic dystrophy
myotonic dystrophy
dynamic mutation
myotonia
Autosomal dominant
spinocerebellar ataxias

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