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Medical Genetics-Mendelian Genetics
Robert F. Waters, Ph.D.
Preparation for Pathology
Preparation for Immunology
Preparation for Epidemiology
Etc.
Gametes
Spermatogenesis
Oogenesis
Chromosomes (Karyotype)
Classification of Chromosomes
Centromeric Classification (Nuclear)
Metacentric (mediocentric)
• Center (nearly)
Submetacentric (submediocentric)
• Little off center
• q-long arm
• p-short arm
Acrocentric
• Centromere at the terminus
Meiosis
First meiotic division
Meiosis
Second meiotic division
Human Spermatogenesis
Human Oogenesis
Intrauterine primary Oocyte
First meiotic division
Second meiotic division
12 to 50 years after start of meiosis
Ova (secondary Oocyte)
• Receives most of the cytoplasm
Others become polar bodies
Longer prophase in meiosis in females
Higher probability of meiotic non-disjunction
The Pedigree
Propositus
P1 (Parental)
F1, F2, etc. (Filial)
Phenylthiocarbamide (PTC)
Taster vs. Non-taster
Homozygous
Heterozygous
Complete dominance
Punnett’s square
Genotype and Phenotype
Genotypic ratio and phenotypic ratio
Autosomal Dominant
Approximately 50% Males and
Females affected
Dentinogenesis imperfecta
Pediatric opalescent brown color
Wear down easily
Dentinogenesis imperfecta
Approximately 1:8000
Criteria for Autosomal
Dominant
Usually not fully expressed in
heterozygous state
Appears in every generation with no
skipping
Trait transmitted by affected person to
half the offspring (average)
Unaffected persons do not transmit the
disease (not carriers)
Occurrence and transmission of trait not
influenced by sex (males ~ females)
Autosomal Recessive
Cystic Fibrosis
Consanguinity and Recessive
Inheritance
Autosomal Recessive-Cont:
Tay-Sachs Disease
Ashkenazi Jews
• Neuro-degenerative disorder
High frequency in North America
• Migrations
Tyrosinemia
Usually lethal
Hepatic lethal
Autosomal Recessive-Cont:
Criteria
Carrier identification, if possible
Trait characteristically occurs in sibs, not in
parents, immediate offspring, and most other
close relatives
About 1 in 4 ratio at birth to have trait
Parents of affected child may be
consanguineous (unknowingly)
Males and females equally likely to be affected
Multiple Alleles
ABO blood type system
Sex Linked Inheritance
X-Linked
May be X-linked Recessive
May be X-linked Dominant
When X-Linked gene in male (y) is
considered hemizygous not
heterozygous
X-Linked Recessive
Follow a well defined pattern
Expressed always males and only in
females that are homozygous
Example (Hemophilia)
Queen Victoria
• Classical Hemophilia A (XR)
• Deficiency in antihemophilic globulin
• Clinical features
• Severe arthritis’
• Internal joint hemorrhages
• Difficulty in healing after cuts or abrasions
X-Linked Recessive
Normal Female
Hemophiliac male
OVA
Xh
y
XH
XH Xh
XHy
XH
XH Xh
XHy
Daughters: 100% carriers (heterozygotes)
Sons: 100% normal
X-Linked Recessive Cont:
Carrier Female
Normal Male
ova
XH
Xh
XH
XH XH XH Xh
y
XHy
Xhy
Daughters: 50% normal, 50% carriers
Sons: 50% normal, 50% affected
Criteria for X-Linked
Recessive Inheritance
Incidence of trait much higher in
males
Trait passed from affected man
through all his daughters to half
their sons
Trait never passed directly from
father to son
X-Linked Dominant
Inheritance
Traits occur approximately twice as
often in females
Affected male transmits the trait to
ALL of his daughters and to NONE of
his sons
X-Linked Dominant Cont:
Example
X-linked blood group system Xg
Xg/Xg x Xga/y Male has Dom. Marker
OVA
Xg
Xg
Xga
Xga/ Xg Xga/Xg
y
Xg/y
Xg/y
Daughters: Gen: Xga/ Xg Phen: Xg(a+) -- Like father
Sons: Gen: Xg/y Phen: Xg(a-) –- like mother
X-Linked Dominant Cont:
Heterozygous female and Xg(a-)male
Cross is Xga/ Xg x Xg/y
Ova
Xg
y
Xga
Xg
Xga/ Xg Xg/Xg
Xga /y Xg/y
Daughters:Xga/ Xg Xg/Xg – 50% receive dominant allele
Sons: Xga /y Xg/y – 50% receive dominant allele
Criteria for X-Linked
Dominant Inheritance
Affected males transmit trait to all of their
daughters but to none of their sons
Affected females who are heterozygous
transmit the gene to half the sons and
half the daughters
In X-Linked dominant disorders, affected
females are twice as common as affected
males but will express the condition
in a milder form (heterozygous)
Penetrance
Ability of any gene to be expressed
When some individuals have the
gene but fail to express it are said to
have reduced penetrance
Patients who have a gene and do
not express it are said to have a
nonpenetrant gene
Expressivity
The degree of expression of a
penetrant gene
Polymorphisms
May be due to modifier genes
E.g. oncorepressor genes repressing
oncogenes
Pleiotropy
One gene, multiple effects
Stem cells
E.g. galactosemia
Defect in galactose-1-phosphate uridyl
transferase
• Multiple effects
•
•
•
•
Cirrhosis of liver
Cataracts
Galactosuria
Mental retardation
Reversed by galactose free diet
Sex-Limited and SexInfluenced Genes
Sex-Limited Trait
Autosomally inherited trait expressed in
one sex (e.g., male only)
X-linked ruled out because may be
transmitted by females
Precocious puberty
• Exhibit adolescent growth spurt around the
age of four years
Precocious Puberty Pedigree
Autosomal dominant precocious
puberty
Sex-Limited Expression
Testicular feminization
XY males have testes but are also born
with female external genitalia and
raised as females (Some female
secondary sexual characteristics at
puberty)
Autosomal Phenotypes with Unequal Male
and Female Expression
Hemochromatosis
May be less expression in young
females
Menstrual cycle
Iron storage disease
Different from Thalassemias
Treatments
Latent Genes (Delayed Onset)
Huntington’s Chorea
Choreic movement
Unpredictable, jerky, ballistic
Mental deterioration
Dominantly inherited
Gene remains in population
After reproductive age
Variable onset
Usually above 35