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Related Concept Videos

Lethal Alleles02:41

Lethal Alleles

Agouti: A Lethal Allele
Lucien Cuénot discovered lethal alleles in 1905 while studying the inheritance of coat color in mice. The agouti gene is responsible for the color of the coat in mice. This gene codes for an agouti-signaling protein, which is responsible for melanin distribution in mammals. The wild-type allele gives rise to gray-brown coat color in mice, while the mutant allele gives rise to yellow coat color. In addition to coat color, the agouti gene is associated with the yellow...
Incomplete Dominance01:43

Incomplete Dominance

Gregor Mendel's work (1822 - 1884) was primarily focused on pea plants. Through his initial experiments, he determined that every gene in a diploid cell has two variants called alleles inherited from each parent. He suggested that amongst these two alleles, one allele is dominant in character and the other recessive. The combination of alleles determines the phenotype of a gene in an organism.
Epistasis Analysis01:09

Epistasis Analysis

Although Mendel chose seven unrelated traits in peas to study gene segregation, most traits involve multiple gene interactions that create a spectrum of phenotypes. When the interaction of various genes or alleles at different locations influences a phenotype, this is called epistasis. Epistasis often involves one gene masking or interfering with the expression of another (antagonistic epistasis). Epistasis often occurs when different genes are part of the same biochemical pathway. The...
Hedgehog Signaling Pathway02:33

Hedgehog Signaling Pathway

The Hedgehog gene (Hh) was first discovered due to its control of the growth of disorganized, hair-like bristles phenotype in Drosophila, much like hedgehog spines. Hh plays a crucial role in the development of organs and the maintenance of homeostasis in both invertebrates and vertebrates. However, while Drosophila has only one Hh protein, mammals have multiple functional Hedgehog proteins - Sonic (Shh), Desert (Dhh), and Indian Hedgehog (Ihh). All of these homologous proteins have adapted to...
Nondisjunction01:29

Nondisjunction

During meiosis, chromosomes occasionally separate improperly. This occurs due to failure of homologous chromosome separation during meiosis I or failed sister chromatid separation during meiosis II. In some species, notably plants, nondisjunction can result in an organism with an entire additional set of chromosomes, which is called polyploidy. In humans, nondisjunction can occur during male or female gametogenesis and the resulting gametes possess one too many or one too few chromosomes.
Nondisjunction01:21

Nondisjunction

Nondisjunction is the failure of homologous chromosomes or sister chromatids to separate correctly and move to the opposite poles of the cells. This produces daughter cells with abnormal chromosome numbers.  Nondisjunction is common during anaphase I or anaphase II of meiosis.  Mutations in synaptonemal complex proteins that attach homologous chromosomes increase the chances of nondisjunction in anaphase I of meiosis I. In contrast, mutations in topoisomerases and condensins that hold sister...

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Related Experiment Video

Updated: Jun 2, 2026

Investigating the Pathogenesis of MYH7 Mutation Gly823Glu in Familial Hypertrophic Cardiomyopathy using a Mouse Model
03:45

Investigating the Pathogenesis of MYH7 Mutation Gly823Glu in Familial Hypertrophic Cardiomyopathy using a Mouse Model

Published on: August 8, 2022

May-Hegglin anomaly in a dog.

Bente Flatland1, Michael M Fry, Seung J Baek

  • 1Department of Pathobiology, College of Veterinary Medicine, University of Tennessee, Knoxville, TN 37996, USA. bflatlan@utk.edu

Veterinary Clinical Pathology
|May 11, 2011
PubMed
Summary

A genetic mutation in the MYH9 gene was identified in a Pug dog with May-Hegglin anomaly (MHA). This discovery marks the first reported MYH9 mutation in dogs, offering insights into MHA-associated macrothrombocytopenia.

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Published on: May 24, 2016

Area of Science:

  • Veterinary Genetics
  • Hematology
  • Canine Pathology

Background:

  • A Pug dog presented with cutaneous lesions secondary to immunosuppressive treatment for presumed immune-mediated thrombocytopenia.
  • Hematologic abnormalities included persistent thrombocytopenia, macrothrombocytes, and characteristic neutrophil inclusions, suggesting May-Hegglin anomaly (MHA).

Observation:

  • Transmission electron microscopy showed normal platelet ultrastructure but neutrophil inclusions resembling those in human MHA.
  • Neutrophil function tests were normal, but thrombelastography revealed prolonged clotting times and impaired platelet response to ADP.

Findings:

  • Immunocytochemistry for MYH9 protein was negative, but DNA sequencing identified a specific point mutation (Q1841K) in the dog's MYH9 gene.
  • This mutation is identical to a known human MHA-associated mutation.
  • This is the first documented MYH9 mutation in a canine case of MHA.

Implications:

  • This finding establishes a genetic basis for MHA in dogs, linked to the MYH9 gene.
  • MHA-associated macrothrombocytopenia can be misdiagnosed as immune-mediated thrombocytopenia, highlighting the need for genetic testing.
  • This research provides a foundation for future studies on MHA in canines and its clinical management.