Essential Information & explanations, latest texts & monographs on
Mendelian_inheritance.
Mendelian inheritance
Mendelian inheritance (or Mendelian genetics or Mendelism) refers to the primary tenets that underly much of genetics developed by Gregor Mendel in the latter part of the 19th century. Mendel (1822-1884), an Austrian monk, was interested in understanding variances in plants, and between 1856 and 1863 cultivated and tested some at [1]) that was read to the Natural History Society of Brunn on February 8 and March 8, 1865, and was published in 1866.
Before Gregor Mendel formulated his theories of genetics in 1865, the prevailing theory of biological inheritance was that of blending inheritance, in which the sperm and egg of parent organisms contained a sampling of the parent's "essence" and that they somehow blended together to form the pattern for the offspring. This theory accounted for the fact that offspring tended to resemble their parents without all members of a population eventually averaging themselves out.
Mendel proposed instead a theory of particulate inheritance, in which characteristics were determined by discrete units of inheritance that were passed intact from one generation to the next. These units would later come to be known as genes, though Mendel did not coin the term himself. Mendel based his theory on experiments involving the cross-pollination between two plants or self-pollinatation with a single plant. Based on many years of careful, tedious breeding experiments, Mendel developed several fundamental laws of Mendelian inheritance.
Mendel's Law of Independent Assortment
The most important principle of Mendel's Law of Independent Assortment is that the emergence of one trait will not affect the emergence of another. While his experiments mixing one trait always resulted in a 3:1 ratio (Fig. 1) between dominant and recessive phenotypes, his experiments with two traits showed 9:3:3:1 ratios (Fig. 2). Mendel concluded that each organism carries two sets of information about its phenotype. If the two sets differ on the same phenotype, one of them dominates the other. That way, information can be passed on through the generations, even if the phenotype is not expressed (F1 generations, figures 1 and 2).
Figure 1 : Dominant and recessive phenotypes.
(1) Parental generation. (2) F1 generation. (3) F2 generation. Dominant (red) and recessive (white) phenotype look alike in the F1 (first) generation and show a 3:1 ratio in the F2 (second) generation
Figure 2 : Two traits (black/white and short/long hair, with black and short dominant) show a 9:3:3:1 ratio in the F2 generation. (S=short, s=long, B=black, b=white hair)
(1) Parental generation. (2) F1 generation. (3) F2 generation.
Results : 9x short black hair, 3x long black hair, 3x short white hair, 1x long white hair.
Mendel's findings allowed other scientists to simplify the emergence of traits to mathematical probability. A large portion of Mendel's spectacular findings can be traced to his made certain to start his experiments only with true breeding plants. He also only measured absolute characteristics such as color, shape, and position of the offspring. His data was expressed numerically and subjected to statistical analysis. This method of data reporting and the large sampling size he used gave credibility to his data. He also had the foresight to look through several successive generations of his pea plants and record their variations. Without his careful attention to procedure and detail, Mendel's work could not have had the impact it made on the world of genetics.
Mendel's Law of Segregation
Mendel's Law of Segregation essentially has four parts.
Alternative versions of genes account for variations in inherited characters. This is the concept of alleles. Alleles are different versions of genes that impart the same characteristic. Each human has a gene that controls height, but there are variations among these genes in accordance with the specific height the gene "codes" for.
For each character, an organism inherits two genes, one from each parent. This means that when somatic cells are produced from two gametes, one allele comes from the mother, one from the father. These alleles may be the same (true-breeding organisms, e.g. ww and rr in Fig. 3), or different (hybrids, e.g. wr in Fig. 3).
If the two alleles differ, then one, the dominant allele, is fully expressed in the organism's appearance; the other, the segregate during gamete production. This is the last part of Mendel's generalization. The two alleles of the organism are separated into different gametes, ensuring variation.
Figure 3 : The color alleles of Mirabilis jalapa are not dominant or recessive.
(1) Parental generation. (2) F1 generation. (3) F2 generation. The "red" and "white" allele together make a "pink" phenotype, resulting in a 1:2:1 ratio of red:pink:white in the F2 generation.
During his experiments, Mendel encountered some traits that did not follow the laws he had encountered. These traits did not appear independently, but always together with at least one other trait. Mendel could not explain what happened and chose not to mention it in his work. Today, we know that these traits are close together on the same chromosome.
The above article is adapted from from Wikipedia All Wikipedia article text is available under the terms of the GNU Free Documentation License
Bibliographic Resources
Updates and comments at Essential Facts blog
Are you interested in Feng Shui?
Price Theory Resources
Fructose, Sucrose, Glucose Core Bibliography
World Class Photographers
Some philosophical movements
Top PDF and eBook Downloads
Recent Mendelian_inheritance related patents
From USPTO:
from PUBMED
1: Hern LM, Bidichandani SI.
What Mendel did not discover: exceptions in Mendelian genetics and their role
in inherited human disease.
J Okla State Med Assoc. 2004 Jan;97(1):12-7.
PMID: 14998061
2: Uhl GR, Grow RW.
The burden of complex genetics in brain disorders.
Arch Gen Psychiatry. 2004 Mar;61(3):223-9.
PMID: 14993109
3: Chow SN, Lin MC, Shen J, Wang S, Jong YJ, Chien CH.
Analysis of chromosome abnormalities by comparative genomic hybridization in
malignant peripheral primitive neuroectodermal tumor of the ovary.
Gynecol Oncol. 2004 Mar;92(3):752-60.
PMID: 14984937
4: Dodgson JB.
Chicken genome sequence: a centennial gift to poultry genetics.
Cytogenet Genome Res. 2003;102(1-4):291-6.
PMID: 14970719
5: Chow S, Scholey VP, Nakazawa A, Margulies D, Wexler JB, Olson RJ, Hazama K.
Direct evidence for Mendelian inheritance of the variations in the ribosomal
protein gene introns in yellowfin tuna (Thunnus albacares).
Mar Biotechnol (NY). 2001 Jan;3(1):22-6.
PMID: 14961386 [PubMed]
6: Maxwell MR, Buresch KM, Hanlon RT.
Pattern of inheritance of microsatellite loci in the squid Loligo pealeii
(Mollusca: Cephalopoda).
Mar Biotechnol (NY). 2000 Nov;2(6):517-21.
PMID: 14961175 [PubMed]
7: Al-Jader LN, Harper PS, Krawczak M, Palmer SR.
The frequency of inherited disorders database: prevalence of Huntington
disease.
Community Genet. 2002 Apr;4(3):148-57.
PMID: 14960907 [PubMed]
8: Rost S, Fregin A, Ivaskevicius V, Conzelmann E, Hortnagel K, Pelz HJ,
Lappegard K, Seifried E, Scharrer I, Tuddenham EG, Muller CR, Strom TM,
Oldenburg J.
Mutations in VKORC1 cause warfarin resistance and multiple coagulation factor
deficiency type 2.
Nature. 2004 Feb 5;427(6974):537-41.
PMID: 14765194
9: Scheuner MT, Yoon PW, Khoury MJ.
Contribution of Mendelian disorders to common chronic disease: opportunities
for recognition, intervention, and prevention.
Am J Med Genet. 2004 Feb 15;125C(1):50-65.
PMID: 14755434
10: Bosch AM, Waterham HR, Bakker HD.
[From gene to disease; galactosemia and galactose-1-phosphate uridyltransferase
deficiency]
Ned Tijdschr Geneeskd. 2004 Jan 10;148(2):80-1. Review. Dutch. Erratum in: Ned
Tijdschr Geneeskd. 2004 Feb 7;148(6):300.
PMID: 14753129
11: Morris RW, Kaplan NL.
Testing for association with a case-parents design in the presence of
genotyping errors.
Genet Epidemiol. 2004 Feb;26(2):142-54.
PMID: 14748014
12: Oostenbrug LE, van Dullemen HM, te Meerman GJ, Jansen PL.
IBD and genetics: new developments.
Scand J Gastroenterol Suppl. 2003;(239):63-8.
PMID: 14743885
13: Cordato DJ, Chan DK.
Genetics and Parkinson's disease.
J Clin Neurosci. 2004 Feb;11(2):119-23.
PMID: 14732367
14: Song Y, Niu T, Manson JE, Kwiatkowski DJ, Liu S.
Are variants in the CAPN10 gene related to risk of type 2 diabetes? A
quantitative assessment of population and family-based association studies.
Am J Hum Genet. 2004 Feb;74(2):208-22. Epub 2004 Jan 13.
PMID: 14730479
15: Cantor MN, Lussier YA.
Putting data integration into practice: using biomedical terminologies to add
structure to existing data sources.
Proc AMIA Symp. 2003;:125-9.
PMID: 14728147
16: Leem SH, Kouprina N, Grimwood J, Kim JH, Mullokandov M, Yoon YH, Chae JY,
Morgan J, Lucas S, Richardson P, Detter C, Glavina T, Rubin E, Barrett JC,
Larionov V.
Closing the gaps on human chromosome 19 revealed genes with a high density of
repetitive tandemly arrayed elements.
Genome Res. 2004 Feb;14(2):239-46. Epub 2004 Jan 12.
PMID: 14718380
17: Winter EE, Goodstadt L, Ponting CP.
Elevated rates of protein secretion, evolution, and disease among
tissue-specific genes.
Genome Res. 2004 Jan;14(1):54-61.
PMID: 14707169
18: Minvielle F, Gourichon D, Monvoisin JL.
Effects of two-locus combinations, using the roux, lavender, and beige
mutations, on plumage color of Japanese quail.
J Hered. 2003 Nov-Dec;94(6):517-22.
PMID: 14691319
19: Stitziel NO, Binkowski TA, Tseng YY, Kasif S, Liang J.
topoSNP: a topographic database of non-synonymous single nucleotide
polymorphisms with and without known disease association.
Nucleic Acids Res. 2004 Jan 1;32 Database issue:D520-2.
PMID: 14681472
20: Wheeler DL, Church DM, Edgar R, Federhen S, Helmberg W, Madden TL, Pontius
JU, Schuler GD, Schriml LM, Sequeira E, Suzek TO, Tatusova TA, Wagner L.
Database resources of the National Center for Biotechnology Information:
update.
Nucleic Acids Res. 2004 Jan 1;32 Database issue:D35-40.
PMID: 14681353
|