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Contents

   



(Top)
 


1 Definition  





2 Genetic origin of traits in diploid organisms  





3 Biochemistry of dominance and extensions to expression of traits  





4 Continuum versus categorical traits  





5 See also  





6 Citations  





7 References  














Phenotypic trait






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From Wikipedia, the free encyclopedia
 

(Redirected from Trait (biology))

Eye color is an example of a (physical) phenotypic trait

Aphenotypic trait,[1][2] simply trait, or character state[3][4] is a distinct variant of a phenotypic characteristic of an organism; it may be either inherited or determined environmentally, but typically occurs as a combination of the two.[5] For example, having eye color is a character of an organism, while blue, brown and hazel versions of eye color are traits. The term trait is generally used in genetics, often to describe phenotypic expression of different combinations of alleles in different individual organisms within a single population, such as the famous purple vs. white flower coloration in Gregor Mendel's pea plants. By contrast, in systematics, the term is character state is employed to describe features that represent fixed diagnostic differences among taxa, such as the absence of tails in great apes, relative to other primate groups.[6]

Definition

[edit]

Aphenotypic trait is an obvious, observable, and measurable characteristic of an organism; it is the expression of genes in an observable way. An example of a phenotypic trait is a specific hair color or eye color. Underlying genes, that make up the genotype, determine the hair color, but the hair color observed is the phenotype. The phenotype is dependent on the genetic make-up of the organism, and also influenced by the environmental conditions to that of the organism is subjected across its ontogenetic development,[7] including various epigenetic processes. Regardless of the degree of influence of genotype versus environment, the phenotype encompasses all of the characteristics of an organism, including traits at multiple levels of biological organization, ranging from behavior and evolutionary history of life traits (e.g., litter size), through morphology (e.g., body height and composition), physiology (e.g., blood pressure), cellular characteristics (e.g., membrane lipid composition, mitochondrial densities), components of biochemical pathways, and even messenger RNA.[citation needed]

Genetic origin of traits in diploid organisms

[edit]

Different phenotypic traits are caused by different forms of genes, or alleles, which arise by mutation in a single individual and are passed on to successive generations.[8]

Biochemistry of dominance and extensions to expression of traits

[edit]

The biochemistry of the intermediate proteins determines how they interact in the cell. Therefore, biochemistry predicts how different combinations of alleles will produce varying traits.[citation needed]

Extended expression patterns seen in diploid organisms include facets of incomplete dominance, codominance, and multiple alleles. Incomplete dominance is the condition in which neither allele dominates the other in one heterozygote. Instead the phenotype is intermediate in heterozygotes. Thus you can tell that each allele is present in the heterozygote.[9] Codominance refers to the allelic relationship that occurs when two alleles are both expressed in the heterozygote, and both phenotypes are seen simultaneously.[10] Multiple alleles refers to the situation when there are more than 2 common alleles of a particular gene. Blood groups in humans is a classic example. The ABO blood group proteins are important in determining blood type in humans, and this is determined by different alleles of the one locus.[11]

Continuum versus categorical traits

[edit]

Schizotypy is an example of a psychological phenotypic trait found in schizophrenia-spectrum disorders. Studies have shown that gender and age influences the expression of schizotypal traits.[12] For instance, certain schizotypal traits may develop further during adolescence, whereas others stay the same during this period.[12]

See also

[edit]

Citations

[edit]
  1. ^ Williams, David; Schmitt, Michael; Wheeler, Quentin (2016-07-21). The Future of Phylogenetic Systematics: The Legacy of Willi Hennig. Cambridge University Press. ISBN 9781107117648.
  • ^ Yeates, David K.; Wiegmann, Brian M. (2005). The Evolutionary Biology of Flies. Columbia University Press. ISBN 9780231127004.
  • ^ "Reconstructing trees: A step by step method – Understanding Evolution". 29 May 2021.
  • ^ Wright, April M; Lloyd, Graeme T; Hillis, David M (2016). "Modeling Character Change Heterogeneity in Phylogenetic Analyses of Morphology through the Use of Priors". Systematic Biology. 65 (4): 602–611. doi:10.1093/sysbio/syv122. PMID 26715586.
  • ^ Lawrence, Eleanor (2005) Henderson's Dictionary of Biology. Pearson, Prentice Hall. ISBN 0-13-127384-1
  • ^ Brower, Andrew V. Z.; Schuh, Randall T. (2021). Biological Systematics: Principles and Applications. Cornell University Press. ISBN 9781501752773.
  • ^ *Campbell, Neil; Reece, Jane, Biology, Benjamin Cummings
  • ^ Gerstein, Mark B.; Bruce, Can; Rozowsky, Joel S.; Zheng, Deyou; Du, Jiang; Korbel, Jan O.; Emanuelsson, Olof; Zhang, Zhengdong D.; Weissman, Sherman; Snyder, Michael (June 2007). "What is a gene, post-ENCODE? History and updated definition". Genome Research. 17 (6): 669–681. doi:10.1101/gr.6339607. ISSN 1088-9051. PMID 17567988.
  • ^ Bailey, Regina. "What is incomplete dominance". About.com.
  • ^ McClean, Philip. "Variations to Mendel's First Law of Genetics".
  • ^ Unknown. "Multiple Alleles".
  • ^ a b Fonseca-Pedrero, Eduardo; Lemos-Giráldez, Serafín; Paino, Mercedes; Sierra-Baigrie, Susana; Muñiz, José (2012-08-01). "Phenotypic Expression of Schizotypal Traits in an Adolescent Population". Journal of Personality Disorders. 26 (4): 539–550. doi:10.1521/pedi.2012.26.4.539. ISSN 0885-579X. PMID 22867505.
  • References

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