Hybrid growth disorders

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Hybrid growth disorders refer to reduced growth or overgrowth in an organism that is a hybrid of two different species. [1] In some sense, it is a type of hybrid dysgenesis when the growth disorder proves deleterious, making it the opposite of heterosis or hybrid vigour. [2] [3]

Hybrid growth disorders may be referred to as a growth dysplasia, especially when resulting in overgrowth, although this terminology may be confusing since the term dysplasia is commonly used to imply an impending cancer. [4] However, a hybrid growth disorder is not caused by cancer.

Hybrid growth disorders are exhibited among a variety organisms, including ligers, tigons, hybrid mice, and hybrid dwarf hamsters. [5] [6]

A study on hybrid mice which investigated the possible causes for hybrid growth disorders reveals genomic imprinting to have a major effect. [6] Paternal imprinting may increase growth to maximize maternal resources allocated to his progeny, while maternal imprinting may suppress growth in favor of ensuring her own survival and equal allocation of resources between offspring. [7] This suggests that the extent of a disorder depends on the combination of parental species and their respective sexes, as demonstrated by the Vrana study. [6] The study concludes that hybrid growth disorders most commonly affect the heterozygous sex, as expected by Haldane's rule. [8] [9] This would also explain why hybrid growth disorders often appear to affect one sex more than the other.

Similarly, a study of hybrids between dwarf hamster species Phodopus campbelli and Phodopus sungorus suggests that gene imprinting causes abnormal interactions between growth-promoting and growth-repressing genes which regulate placental and embryonic growth. [1]

See also

Related Research Articles

Genomic imprinting is an epigenetic phenomenon that causes genes to be expressed in a parent-of-origin-specific manner. Genes however, can also be partially imprinted. Partial imprinting happens when alleles from both parents are differently expressed rather than complete expression and complete suppression of one parent's allele. Forms of genomic imprinting have been demonstrated in fungi, plants and animals. As of 2014, there are about 150 imprinted genes known in the mouse and about half that in humans. In 2019, 260 imprinted genes have been reported in mice and 228 in humans.

Selfish genetic elements are genetic segments that can enhance their own transmission at the expense of other genes in the genome, even if this has no positive or a net negative effect on organismal fitness. Genomes have traditionally been viewed as cohesive units, with genes acting together to improve the fitness of the organism. However, when genes have some control over their own transmission, the rules can change, and so just like all social groups, genomes are vulnerable to selfish behaviour by their parts.

Achondroplasia is a genetic disorder whose primary feature is dwarfism. In those with the condition, the arms and legs are short, while the torso is typically of normal length. Those affected have an average adult height of 131 centimetres for males and 123 centimetres (4 ft) for females. Other features include an enlarged head and prominent forehead. Complications can include sleep apnea or recurrent ear infections. The disorder does not generally affect intelligence.

Dwarfism Small size of an organism, caused by growth deficiency or genetic mutations

Dwarfism occurs when an organism is extremely small. In humans, it is sometimes defined as an adult height of less than 147 centimetres, regardless of sex; the average adult height among people with dwarfism is 122 centimetres, although some individuals with dwarfism are slightly taller. Disproportionate dwarfism is characterized by either short limbs or a short torso. In cases of proportionate dwarfism, both the limbs and torso are unusually small. Intelligence is usually normal, and most have a nearly normal life expectancy.

Megalencephaly

Megalencephaly is a growth development disorder in which the brain is abnormally large. It is characterized by a brain with an average weight that is 2.5 standard deviations above the mean of the general population. Approximately 1 out of 50 children (2%) are said to have the characteristics of megalencephaly in the general population.

Haldanes rule

Haldane's rule is an observation about the early stage of speciation, formulated in 1922 by the British evolutionary biologist J.B.S. Haldane, that states that if in a species hybrid only one sex is inviable or sterile, that sex is more likely to be the heterogametic sex. The heterogametic sex is the one with two different sex chromosomes; in therian mammals, for example, this is the male.

Heterosis, hybrid vigor, or outbreeding enhancement is the improved or increased function of any biological quality in a hybrid offspring. An offspring is heterotic if its traits are enhanced as a result of mixing the genetic contributions of its parents. These effects can be due to Mendelian or non-Mendelian inheritance.

Ellis–Van Creveld syndrome

Ellis–Van Creveld syndrome is a rare genetic disorder of the skeletal dysplasia type.

Testis-determining factor Protein that initiates male sex determination in therian mammals

Testis-determining factor (TDF), also known as sex-determining region Y (SRY) protein, is a DNA-binding protein encoded by the SRY gene that is responsible for the initiation of male sex determination in therian mammals. SRY is an intronless sex-determining gene on the Y chromosome. Mutations in this gene lead to a range of disorders of sex development (DSD) with varying effects on an individual's phenotype and genotype.

X-inactivation Inactivation of copies of X chromosome

X-inactivation is a process by which one of the copies of the X chromosome is inactivated in therian female mammals. The inactive X chromosome is silenced by it being packaged into a transcriptionally inactive structure called heterochromatin. As nearly all female mammals have two X chromosomes, X-inactivation prevents them from having twice as many X chromosome gene products as males, who only possess a single copy of the X chromosome.

Pleiotropy Influence of a single gene on multiple phenotypic traits

Pleiotropy occurs when one gene influences two or more seemingly unrelated phenotypic traits. Such a gene that exhibits multiple phenotypic expression is called a pleiotropic gene. Mutation in a pleiotropic gene may have an effect on several traits simultaneously, due to the gene coding for a product used by a myriad of cells or different targets that have the same signaling function.

Agenesis of the corpus callosum (ACC) is a rare birth defect in which there is a complete or partial absence of the corpus callosum. It occurs when the development of the corpus callosum, the band of white matter connecting the two hemispheres in the brain, in the embryo is disrupted. The result of this is that the fibers that would otherwise form the corpus callosum are instead longitudinally oriented along the ipsilateral ventricular wall and form structures called Probst bundles.

P elements are transposable elements that were discovered in Drosophila as the causative agents of genetic traits called hybrid dysgenesis. The transposon is responsible for the P trait of the P element and it is found only in wild flies. They are also found in many other eukaryotes.

Simpson–Golabi–Behmel syndrome X-linked disease characterized by pre- and postnatal overgrowth and craniofacial, skeletal, cardiac and renal abnormalities

Simpson–Golabi–Behmel syndrome (SGBS), is a rare inherited congenital disorder that can cause craniofacial, skeletal, cardiac, and renal abnormalities. The syndrome is inherited in an X-linked recessive fashion, where males express the phenotype and females usually do not. Females that possess one copy of the mutation are considered to be carriers of the syndrome and may express varying degrees of the phenotype.

Ectrodactyly–ectodermal dysplasia–cleft syndrome

Ectrodactyly–ectodermal dysplasia–cleft syndrome, or EEC, and also referred to as EEC syndrome and split hand–split foot–ectodermal dysplasia–cleft syndrome is a rare form of ectodermal dysplasia, an autosomal dominant disorder inherited as a genetic trait. EEC is characterized by the triad of ectrodactyly, ectodermal dysplasia, and facial clefts. Other features noted in association with EEC include vesicoureteral reflux, recurrent urinary tract infections, obstruction of the nasolacrimal duct, decreased pigmentation of the hair and skin, missing or abnormal teeth, enamel hypoplasia, absent punctae in the lower eyelids, photophobia, occasional cognitive impairment and kidney anomalies, and conductive hearing loss.

Imprinted brain hypothesis Conjecture on the causes of autism and psychosis

The imprinted brain hypothesis is an unsubstantiated hypothesis in evolutionary psychology regarding the causes of autism spectrum and schizophrenia spectrum disorders, first presented by Bernard Crespi and Christopher Badcock in 2008. It claims that certain autistic and schizotypal traits are opposites, and that this implies the etiology of the two conditions must be at odds.

Cognitive genomics is the sub-field of genomics pertaining to cognitive function in which the genes and non-coding sequences of an organism's genome related to the health and activity of the brain are studied. By applying comparative genomics, the genomes of multiple species are compared in order to identify genetic and phenotypical differences between species. Observed phenotypical characteristics related to the neurological function include behavior, personality, neuroanatomy, and neuropathology. The theory behind cognitive genomics is based on elements of genetics, evolutionary biology, molecular biology, cognitive psychology, behavioral psychology, and neurophysiology.

Autism spectrum disorder (ASD) includes autism, Asperger disorder, childhood disintegrative disorder and pervasive developmental disorder not otherwise specified. While the exact cause of ASD has remained somewhat of a mystery, it appears to be genetic in origin. Most data supports a polygenic, epistatic model, meaning that the disorder is caused by two or more genes and that those genes are interacting in a complex manner. Several genes, between two and fifteen in number, have been identified and could potentially contribute to disease susceptibility. However, an exact determination of the cause of ASD has yet to be discovered and there probably is not one single genetic cause of any particular set of disorders, leading many researchers to believe that epigenetic mechanisms, such as genomic imprinting or epimutations, may play a major role.

45,X/46,XY mosaicism, also known as X0/XY mosaicism and mixed gonadal dysgenesis, is a rare disorder of sex development in humans associated with sex chromosome aneuploidy and mosaicism of the Y chromosome. This is called a mosaic karyotype because, like tiles in mosaic floors or walls, there is more than one type of cell. It is a fairly rare chromosomal disorder, with an estimated incidence rate of about 1 in 15,000 live births.

Eric Vilain

Eric Vilain is a physician-scientist and professor in the fields of Disorders/Differences of Sex Development (DSDs) and precision medicine. He has been the director of the Center for Genetic Medicine Research at Children’s National Medical Center and the chair of the Department of Genomics and Precision Medicine at the George Washington University School of Medicine & Health Sciences in Washington, D.C. since 2017. Vilain is a fellow of the American College of Medical Genetics, serves on the International Olympic Committee’s Medical Commission, and sits on the Board of Scientific Counselors for the National Institute of Child Health and Human Development (NICHD).

References

  1. 1 2 Brekke, Thomas D.; Good, Jeffrey M. (November 2014). "Parent-of-origin growth effects and the evolution of hybrid inviability in dwarf hamsters". Evolution. 68 (11): 3134–3148. doi:10.1111/evo.12500. PMC   4437546 . PMID   25130206.
  2. ↑ "Definition-hybrid dysgenesis". Life Science Glossary. Northwestern University. Retrieved November 2, 2017.
  3. ↑ Jinks, J. L. (1983). "Biometrical Genetics of Heterosis". Heterosis. Monographs on Theoretical and Applied Genetics. 6. Springer, Berlin, Heidelberg. pp. 1–46. doi:10.1007/978-3-642-81977-3_1. ISBN   9783642819797.
  4. ↑ Dorland's illustrated medical dictionary. Dorland, W. A. Newman (William Alexander Newman), 1864-1956. (32nd ed.). Philadelphia, PA: Saunders/Elsevier. 2012. ISBN   9781416062578. OCLC   706780870.CS1 maint: others (link)
  5. ↑ P., Gray, Annie (1972). Mammalian hybrids: a check-list with bibliography (2d [rev.] ed.). Slough: Commonwealth Agricultural Bureaux. ISBN   978-0851981703. OCLC   532895.
  6. 1 2 3 Paul B. Vrana; et al. (2000). "Genetic and epigenetic incompatibilities underlie hybrid dysgenesis in Peromyscus". Nature Genetics. 25 (1): 120–124. doi:10.1038/75518. PMID   10802670. S2CID   10576141.
  7. ↑ "Genomic Imprinting". learn.genetics.utah.edu. Retrieved 2017-11-10.
  8. ↑ Haldane, J.B.S. (October 1922). "Sex ratio and unisexual sterility in hybrid animals". Journal of Genetics. 12 (2): 101–109. doi:10.1007/BF02983075. S2CID   32459333.
  9. ↑ Delph, Lynda F.; Demuth, Jeffery P. (September 2016). "Haldane's Rule: Genetic Bases and Their Empirical Support". Journal of Heredity. 107 (5): 383–391. doi: 10.1093/jhered/esw026 . PMID   27233288.


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