2010 January

This group of disorders can be classified into 4 categories
- disorders caused by mutations in mitochondrial genes
- diseases caused by triplet-repeat mutations
- disorders associated with genomic imprinting
- disorders associated with gonadal mosaicism
Mitochondrial Gene Disorders
Though most mitochondrial proteins are encoded by nuclear genomes, human
mitochondria contain about 2 – 10 copies of a circular double stranded DNA which code for
several proteins in the mitochondria. These mitochondrial chromosomes are self-replicating
and encode several enzymes involved in oxidative phosphorylation.
Mitochondrial DNA of the zygote is derived exclusively from the oocyte so that
Mitochondrial gene disorders have a maternal form of inheritance. Mutations in copies of
mtDNA are passed on randomly to subsequent generation of cells so that during growth of the
fetus later, it is possible to contain virtually only mutant genomes (mutant homoplasmy),
whereas others have only normal ones (wild-type homoplasmy). Most others will have a
mixed population of mutant and normal mtDNA (heteroplasmy). For this reason, clinical
expression of a disease produced by a given mutation of mtDNA depends on the total content
of mitochondrial genomes and the proportion that is mutant. The fraction of mutant mtDNA
must exceed a critical value for a mitochondrial disease to become symptomatic. This
threshold varies in different organs and is related to the energy requirements of the cells.
Clinically important mitochondrial DNA mutations are rare. Diseases caused by
mutations in the mitochondrial genome principally affect the nervous system, heart and
skeletal muscle. The functional deficits in all these disorders can be traced to oxidative
phosphorylation (so called OXPHOS diseases. OXPHOS diseases can arise from nuclear
mutations and from mtDNA mutations).
The first to be described example of mitochondrial gene disorder is Leber’s
hereditary optic neuropathy. This is a neurodegenerative disorders that manifest itself as
progressive bilateral loss of central vision. It leads in due course to blindness. Other examples
are some of the so-called encephalomyopathies including Kearns-Sayre syndrome.
Triplet-Repeat Mutation diseases
These diseases are due to mutations which are characterized by a long repeating
sequence of three nucleotides. Although the specific nucleotide sequence that undergoes
amplification differs from one disease to another, in most cases the affected sequences share
the nucleotides guanine (G) and cytosine (C).
The prototype of this group is the fragile X syndrome

FRAGILE X SYNDROME
This is the second most common genetic cause of mental retardation.
The genetic defect lies at the distal end of the long arm of the X chromosome. Careful
examination of the karyotype of affected individuals’ lymphocytes, cultured in a folatedepleted
and thymidine-depleted medium, reveals a constriction followed by a thin strand of
genetic material that extends beyond the long arm at the highly conserved band Xq27.3. This
constriction and thin strand produce the appearance of a fragile portion of the X chromosome,
leading to the term fragile X.
The function of the band Xq27.3, which is also termed the fragile X mental
retardation-1 (FMR1) gene, is to synthesize fragile X mental retardation protein (FMRP), a
regulatory protein that binds messenger RNA (mRNA) in neurons and dendrites. In patients
with a full mutation in the FMR1 gene, FMRP is not manufactured because of
hypermethylation of FMR1, and brain development is impaired primarily because of
abnormal synapse connections. FMRP is present in other tissues; however, its role is less
understood.
Once identified and sequenced, the gene was discovered to contain a repeating base
pair triplet (CGG) expansion, which is responsible for fragile X syndrome. Unaffected
individuals have 5-54 CGG repeats in the first exon at the 5′ end of band Xq27.3. A span of
55-200 repeats is known as a premutation, whereas more than 200 repeats is a full mutation.
The defect is dynamic; the number of repeats is unstable from generation to
generation, making the pattern of inheritance difficult to predict.
Males with a full mutation have fragile X syndrome. Mothers of all males with fragile
X syndrome have premutation or fragile X syndrome. Males with fragile X syndrome pass a
premutation to their daughters because sperm cells are mosaics. Sons are unaffected because
they receive the Y chromosome from their fathers.
Males with a premutation are usually unaffected to mildly affected and transmit the
premutation to their daughters. The mutation is stable; thus, the CGG triplets are not
increased. Sons of affected males are unaffected because they receive the Y chromosome
from their fathers.
*Females with a premutation are usually unaffected to mildly affected. Unlike their
male counterparts, the CGG triplets are unstable and increase in size during oogenesis. If the
number of repeats exceeds 200 and the oocyte is fertilized, a male child will have fragile X
syndrome, and a female child will have a 50% chance of having fragile X syndrome. The
number of repeats is directly proportional to the risk of the disorder in an offspring.
Other examples of triple-repeat mutation diseases include Friedrich ataxia, Myotonic
dystrophy, Huntington disease, and various types of spinocerebellar ataxia
Gonadal mosaicism
This results from mutations that occur postzygotically during embryonic development.
If the mutations affect only cells destined for the gonads, the gametes carry the mutation but
the somatic cells of the individual are completely normal. This accounts for many cases of
appearance of, for example, an autosomal dominant condition in an offspring of normal
parents, eg in osteogenesis imparfecta, and these parents may have more than one affected
offspring.
Genomic imprinting
Functional differences have been shown to exist in allelic pairs of certain genes
between the one of paternal origin and the one of maternal origin. These differences result
from an epigenetic process, called imprinting. In most cases, imprinting selectively inactivates
either the paternal or maternal allele.
Prader-Willi syndrome and Angelman syndrome are examples; these two disease
result from an interstitial deletion of band 15q12. When this deletion occurs on the paternal
allele, Prader-Willi syndrome results, while deletion of the same on the maternal allele
produces Angelman syndrome.
Features of Prader-Willi syndrome includes mental retardation, short stature,
hypotonia, obesity, small hands and feet and hypogonadism. Patients with Angelman have
mental retardation, ataxia, seizures, and inappropriate laughter.

These result from combined actions of environmental influences and 2 or more
mutant genes having additive effect. A number of phenotypic characteristics are governed by
this pattern of inheritance eg height, skin colour, IQ, hair colour etc.
The concept of multifactorial inheritance is based on the notion that multiple genes
interact with various environmental factors to produce disease in an individual. Such
inheritance leads to familial aggregation that does not obey simple Mendelian rules. The rist
of expressing a multifactorial disorder is conditioned by the number of mutant genes
inherited; the probability of symptoms in first-degree relatives of a person affected with a
multifactorial disease is usually about 5 – 10%. The probability is considerable lower in
second-degree relatives.
The identical twin concordance rate, which is an indication of the relative role of the
genes versus environmental factors in the genesis of the disease, is usually significantly less
than 100% in multifactorial disorders. For most conditions, it is usually in the range of 20-
40%.
Examples include DM, gout, hypertension, atherosclerosis, coronary heart disease,
cleft lip/palate, congenital heart disease, psoriasis, breast carcinoma etc

Mendelian disorders are expressed single gene mutations that have a large effect.
A mutation is a permanent change in DNA. Mutations may occur in chromosomes
leading to alterations in structure, (as discussed earlier) or in the genes.
Gene mutations are submicroscopic and occur in 2 forms.
i. Point mutations
ii. Frame shift mutations
Point mutation is a situation in which a single nucleotide is substituted by another.
When this occurs in a coding sequence of the DNA, it may result in the replacement of one
amino acid by another in the gene protein product (a situation refered to as missense
mutation), or the new codon may code for the same amino acid (called synchronous
mutations, which will be clinically insignificant), or it may change an amino acid codon to a
chain termination, or stop, codon (a nonsense mutation).
A missense mutation is what occurs in what occurs in sickle cell anaemia while Bthalasssaemia
is an example of nonsense mutation.
In a situation in which the point mutation occurs in a non-coding sequence e.g. in the
promoter and enhancer sequences near a gene, it may affect adversely the expression of that
gene eg in B+ thalasemmia. Point mutations within introns lead to defective splicing and
hence an abnormal product.
Frame shift mutations result from insertions and deletions. This leads to alteration in
the reading frame of the DNA strand. If the number of bases involved is 3 or multiples
thereof, then a frame shift does not occur; rather an abnormal protein with extra amino acids
is synthesized.

CLASSIFICATION
Mendelian disorders can be grouped based on their transmission patterns into 3
classes:
i. Autosomal dominant
ii. Autosomal recessive
iii. Sex linked (or X-linked) disorders.
Although gene expression is usually described as dominant or recessive, in some cases
both alleles of a gene pair may be fully expressed in the individual, a condition called codominance.
eg MHC genes, blood group genes.
More definitions.
Pleitropism – is a situation in which a single mutant gene leads to many end effect.
An example is Sickle Cell disease in which there is hemolysis, organ infarcts, bone changes
etc., Marfan’s syndrome with changes in the CVS, skeleton, eyes etc.
Genetic heterogeneity – this is the opposite of pleiotropism. Here several genetic loci
produce the same traits. For example, Albinism and profound childhood deafness.

AUTOSOMAL DOMINANT DISORDERS.
These are manifested in the heterozygous state. Usually at least one parent of an index
case is affected. Both males and females are affected and both can transmit the condition. On
average, 50% of the offspring of an affected individual will be affected. When a disorder in a
particular is due to a new mutation, none of the parents will be affected.
Two factors may modify the clinical features. These are reduced penetrance and
variable expressivity. Reduced penetrance means that less than 100% of individuals who
inherit the mutant gene express the trait. Penetrance can be described as the proportion
exhibiting the trait amongst those who inherit the mutant gene. It is expressed in %.
For reasons of reduced penetrance, it follows that some phenotypically normal persons
may transmit an autosomal dominant disorder.
Variable expressivity describes a situation in which the features, though seen in all
individuals with the abnormal gene, are expressed differently among them.
In many AD conditions, age of onset of the disorders is delayed. An example is
ADPKD.
AD disorders usually affect structural and regulatory proteins (the latter include carrier
and receptor proteins) and generally tend to be less severe than the recessive disorders.
Examples of AD disorders include:
1. Neurofibromatosis.
2. Adult PKD
3. Familial adenomatuous polyposis coli.
4. Hereditary Spherocytosis
5. Von Willebrand’s diease
6. Marfan syndrome
7. Familial hypercholesterolemia

AUTOSOMAL RECESSIVE DISORDERS
This represents the single largest group of Mendelian disorders. Affected individuals
have mutations in both members of a gene pair, ie homozygous states. Usually, each parent is
a carrier and is unaffected. The occurrence risk when both parents are heterozygous is 25%
for each birth.
The expression of the defect tends to be more uniform than in AD disorders; complete
penetrance is common and onset is frequently early in life.
Many autosomal recessive traits affect enzyme proteins, which have a large safety
margin so that a reduction from the normal 100% activity to 50 in heterozygous persons does
not result in disease.
The chance of having a child with an autosomal recessive disorders is increased if the
parents are blood relatives (consanguinity). Although not a prerequisite, consanguinity is an
important clue that a disease is due to an AR trait.
As mentioned earlier, enzyme proteins are involved in many AR disorders among
which are all inborn errors of metabolism (glycogen storage diseases, mucolipidoses,
lysosomal storage diseases etc.), congenital adrenal hyperplasias, Other proteins that may be
affected in AR disorders include plasma proteins and hemoglobins. Examples of AR include
hemoglobinopathies, thalasemias and childhood PKD.

SEX-LINKED DISORDERS
All sex-linked disorders are X-linked (the Y chromosomes carries very little genetic
14
information almost all of which have to with determination of testes formation and with
spermatogenesis; consequently anomalies associated with these genes lead to infertility and
are therefore not transmissible). Almost all of these sex-linked disorders are recessive.
In the male, the X chromosome is paired with the non-identical partner Y; males
carrying X-linked mutant genes are therefore said to be hemizygous. X-linked recessive
disorders usually manifest in males whereas heterozygous females are carriers. Sons of the
carrier mother have a 50% chance of receiving the mutant gene and therefore manifesting the
disease while the same risk befalls the daughters but they end up as carriers. It is
understandable therefore that X-linked recessive disorders tend to show consistent male
severity in the family; female carriers are usually normal but may be occasionally mildly
affected because of the inactivation of one of the chromosomes in lyonization. If the mutant
gene is kept active in many of the cells in the target tissue then a moderate degree of disease
may result.
Examples include:
Hemophilia A, Hemophilia B, Red-Green colour blindness, Bruton’s
agammaglobulinaemia, G6PD deficiency, Duchenne’s muscular dystrophy, chronic
granulomatous disease etc.

Imbalance of sex chromosomes is much better tolerated than those of autosomes. This
is mainly due to lyonization of all but one X chromosomes and the small amount of genetic
material carried by the Y chromosome.
Lyonization refers to the inactivation of an X chromosome. This is outlined by the
Lyon’s hypothesis. The Lyon hypothesis states that:
i. only one of the X chromosomes in any cell is genetically active,
ii. the other X is rendered inactive.
iii. Inactivation of either paternal or maternal X occurs at random in all cells of the
blastocyst on or about the 16th day of life.
iv. This inactivation persists in all cells derived from each precursor cell.
The inactivated X can be seen in the interphase nucleus as the Barr body or X
chromatin.
Since the Lyon hypothesis was first outlined in 1961, a few modifications have been
made. It is believed now that expression of some genes from both X chromosomes is
necessary for normal growth and development. It has been shown that many X genes escape
inactivation (21% of genes on Xp and 3% of genes on Xq). Also both X chromosomes are
required for normal oogenesis.
The gene responsible for the process of lyonization is the Xist gene; the Xist allele is
turned off in the active X.
The Y-chromosomes is both necessary and sufficient for male development;
regardless of the number of X chromosomes, the presence of a single Y chromosomes
determines the male sex.
Sex chromosomes disorders generally induce subtle chronic problems that relate to
sexual development and fertility. Many are first recognized at the time of puberty. Significant
mental retardation is not usual with them but, in general, the higher the number of X
chromosomes in both male and female, the higher the likelihood of mental retardation.

TURNER SYNDROME

This is characterized by hypogonadism in phenotypic females. It results from complete or partial monosomy of the X chromosomes. About 57% of patients have a complete monosomy with a 45X karyotype. These 45X patients represent only about 1% of fetuses with the 45X karyotype; most conception with this complete monosomy do not survive to birth. The remaining cases of Turner syndrome, one third have partial monosomies which include deletions of varying portions of the X chromosomes with formation of ring chromosomes and isochromosomes, while two thirds are mosaics (eg 45X/47XXX, 45X/46XY). Patients with monosomy X are usually severely affected and with them diagnosis can often be made at birth or in early childhood, while in the other cases (ie mosaics and deletions), they may have an almost normal appearance and may present only with primary amenorhoea. Clinical features Presentation in infancy is with lymph stasis leading to edema of the hands and feet, and sometimes swelling of the nape of the neck (Here, a cystic hygroma, may be produced). Adolescents and adults present with webbing of the neck, short stature (rarely above 1.5m), and at puberty there is failure to develop normal secondary sexual characteristics. The genitalia remain infantile. Turner syndrome is the single most important cause of primary amenorrhoea. In the ovaries, accelerated loss of oocyte, beginning in utero, is complete by the age of 2 years. The ovaries are atrophic, fibrous, devoid of ova and follicles, and are called streak ovaries. Reduced estrogen output leads to high levels of pituitary gonadotrophins. Other features include broad chest with widely spaced nipples, pigmented nevi of skin and a marked carrying angle (cubitus valgus). Congenital heart disorders are also common particularly preductal coarcation of the aorta and aorta stenosis with endocardial fibroelastosis.

KLINEFELTER SYNDROME

KS is male hypogonadism occurring due to the presence of 2 or more X chromosomes in the presence of one or more Y chromosomes. eg XXY, XXXY. It is one of the most common causes of male hypogonadism and can rarely be  diagnosed before puberty. It is a principal cause of male infertility. The incidence of the syndrome is about 1 in 850 live male births. 82% of cases have the classic 47XXY; a little more than half of these result from paternal meiotic nondisjunction resulting in formation of an XY sperm while the remainder is of maternal abnormal XX ovum. Most other cases are mosaics with mostly 46XY/47XXY. Rare cases have 48XXXY or even 49XXXXY, these individuals with multiple X have further physical abnormalities including cryotorchidism, hypospadias, more severe testicular hypospadias, and skeletal changes such as prognathism and radioulnar synostosis. The consistent feature is hypogonadism with severely reduced or completely absence spermatogenesis. The testes show atrophic changes often associated with a small penis. There is lack of secondary male sexual characteristics (such as deep voice, beard, male distribution of pubic hair) and there is also a eunuchoid body habitus with abnormally long legs. Plasma gonatotropin levels are elevated whereas testosterone levels are variably reduced. Mean plasma estradiol levels are also elevated. IQ may be slightly reduced but there is usually no mental retardation. Others Supernumerary Y chromosomes may be found in the male, and multiple X in females (XXX); nearly all are phenotypically normal.

SEXUAL AMBIGUITY.

The sex of an individual is defined at various levels. i) Genetic sex is determined by the presence or absence of a Y chromosome. ii) Gonadal sex is based on the histologic characteristics of the gonads ie testicular or ovarian tissue. iii) Ductal sex depends on the presence of derivatives of the Mullerian or Wolffian ducts iv) Phenotypic or genital sex describes the external genitalia. Sexual ambiguity is present if there is a disagreement among these criteria for sex determination. True hermaphroditism means the presence of both ovarian and testicular tissue. Pseudohermaphroditism represents a disagreement between genital and gonadal sex. A male pseudohermaphrodite has testicular tissue but female genitalia. In female pseudohermaphroditism the genetic sex in all cases is XX and the development of ovaries and 11 internal gentalia is normal. Virilization of the external genitalia result from excessive exposure to androgenic steroids during the early part of gestation. The steroids are usually secreted by fetal adrenal gland affected by congenital adrenal hyperplasia. In male pseudohermaphroditism, there is a Y chromosome so that the gonads are testes but the genital ducts and external genitalia are incompletely differentiated along the male form. The external genitalia may be completely female. It has a multiplicity of causes but common to all is defective virilization of the male embryo, which usually results from genetically determined defects of androgen synthesis, actions or both. The most common form, called complete androgen insensitivity syndrome (or testicular feminization), results from mutation in the gene for the androgen receptor located on the long arm of X.

Down Syndrome.
Also known as mongolism, this is the most common of the chromosomes disorders.
About 95% have trisomy 21 (47XX or XY,+21). 4% have 46 chromosomes but with a
Robertsonian translocation, while about 1% are mosaics.
In the 95 with trisomy 21, meiotic non-disjunction is the most common cause. The
parents are usually normal in all respects. In most of these cases (about 95%), the extra
chromosome-21 is of maternal origin. Increasing maternal age has a very strong effect on the
risk. Mothers about 45 years have a 1 in 25 chance of having a Down syndrome baby. The
cases with robertsonian translocation tend to be familial with one of the parents being a
carrier of the translocation. Symptoms are milder in the mosaics. Maternal age is obviously of
no relevance in these last 2 groups.
Clinical features include:
a. Flat facial profile, oblique palpebral features and epicanthic folds. Brushfield spots
are found on the iris. A prominent tongue, which typically lacks a central fissure, protrudes
from an open mouth.
b. Profound mental retardation. IQ deteriorates over the first decade of life to a mean
of about 30.
c. About 40% have congenital heart defects, eg ASD, VSD, AV valve malformations.
This accounts for the majority of deaths in infancy and childhood.
d. There is a 10 to 20 fold increased in the risk of developing acute leukemia.
e. Virtually all patients with trisomy 21 above 40 years develop changes of
Alzheimer’s disease.
f. Patients are predisposed to serious infections and thyroid autoimmunity due to
abnormal immune responses.
g. GI disorders like duodenal stenosis, imperforate anus and Hirshsprung disease
occur in 2 –3 % of the children.
h. Men with trisomy 21 are invariably sterile due to arrested spermatogenesis.
Trisomy 18 (Edward syndrome)
Other trisomies eg 18 and 13 (Patau’s) are also related to maternal age. Malformations
are more severe than in down’s. Only rarely do the infant survive beyond the first year of life.
Most succumb within a few weeks.
Features of trisomy 18 include mental retardation, prominent occiput, micrognathia,
heart defects, renal malformations and rocker bottom feet. Many of these features are also
found in trisomy 13 where polydactyly and cleft lip and palate are the most characteristic
external manifestations.
Cri du Chat syndrome (del 5p).
This was so named because affected infants up to the age of one year have
characteristic cry of a cat. The often survive into adult life by which time the vocal
characteristics improve. Other features include severe mental retardation, microcephaly and
round face.
22q11 deletion syndrome.
DiGeorge’s syndrome and velocardiofacial syndrome were 2 clinically different
disorders with sometimes overlapping features. Both are characterized by the presence of a
deletion of a portion of the long arm of chromosomes 22 in the band 1 or region 1. They are
now grouped together under the above name.
DiGeorge’s was characterized by thymic hypoplasia with resultant T-cell deficiency,
parathyroid hypoplasia leading to hypocalcemia. VCF was characterized by facial
dysmorphism, cardiovascular anomalies and learning disabilities.
The acronym CATCH 22 was coined to describe this deletion syndrome (Cardiac
abnormalities, Abnormal face, T cell deficit, Cleft palate and Hypocalcaemia).

One of the most extraordinary things connected with Applied Science is the method by which the Navigator is enabled to find the exact spot of sea on which his ship rides. There may be nothing but water and sky within his view; he may be in the midst of the ocean, or gradually nearing the land; the curvature of the globe baffles the search of his telescope; but if he have a correct chronometer, and can make an astronomical observation, he may readily ascertain his longitude, and know his approximate position—how far he is from home, as well as from his intended destination. He is even enabled, at some special place, to send down his grappling-irons into the sea, and pick up an electrical cable for examination and repair.

This is the result of a knowledge of Practical Astronomy. “Place an astronomer,” says Mr. Newcomb, “on board a ship; blindfold him; carry him by any route to any ocean on the globe, whether under the tropics or in one of the frigid zones; land him on the wildest rock that can be found; remove his bandage, and give him a chronometer regulated to Greenwich or Washington time, a transit instrument with the proper appliances, and the necessary books and tables, and in a single clear night he can tell his position within a hundred yards by observations of the stars. This, from a utilitarian point of view, is one of the most important operations of Practical Astronomy.”

. It may be finally said of John Harrison, that by his invention of the chronometer—the ever-sleepless and ever-trusty friend of the mariner—he conferred an incalculable benefit on science and navigation, and established his claim to be regarded as one of the greatest benefactors of mankind.

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