Biology II

CHAPTER 14 Notes

THE CHROMOSOMAL BASIS OF INHERITANCE

LECTURE NOTES:

I. Mendelian inheritance has it s physical basis in the behavior of chromosomes during sexual life cycles

Genetics	Cytology
1860’s: Mendel proposed that discrete inherited factors segregate and assort independently during gamete formation
	1875: Cytologists worked out process of mitosis
	1890: Cytologists worked out process of meiosis
1900: Three botanists (Correns, de Vries and von Seysenegg) independent assortment

1902: Cytlogy and genetics converged as Walter Sutton, Theodor Boveri and others noticed parallels between the behavior of Mendel’s factors and the behavior of chromosomes.

For example:

Ø Chromosomes and genes are both paired in diploid cells.

Ø Homologous chromosomes separate and allele pairs segregate during meiosis.

Ø Fertilization restores the paired condition for both chromosomes and genes.

Based upon these observations, biologists developed the chromosome theory of inheritance.

According to this theory:

Ø Mendelian factors or genes are located on chromosomes.

Ø It is the chromosomes that segregate and independently assort.

II. Morgan traced a gene to a specific chromosome: science as a process

Thomas Hunt Morgan from Columbia University performed experiments in the early 1900’s which provided convincing evidence that Mendel’s inheritable factors are located on chromosomes.

Morgan selected the fruit fly, Drosophila melanogaster, as the experimental organism because these flies:

Ø Are easily cultures in the laboratory.

Ø Are prolific breeders.

Ø Have a short generation time.

Ø Have only four pairs of chromosomes which are easily seen with a microscope.

There are three pairs of autosomes (II, III and IV) and one pair of sex chromosomes. Females have two X-chromosomes, and males have one X and one Y chromosome.

A. A Note on Genetic Symbols

Morgan and his colleagues used genetic symbols that are now convention. For a particular character:

Ø A gene’s symbol is based on the first mutant, non-wild type discovered.

Þ If the mutant is recessive, the first letter is lowercase. (e.g. w = white eye allele in Drosophila.)

Þ If mutant is dominat, the first letter is capitalized. (e.g. Cy = “curly” allele in Drosopjila that causes abnormal, curled wings.)

Ø Wild-type trait is designated by a superscript +. (Cy ⁺ = allele for normal, straight wings.)

Wild type = Normal or most frequently observed phenotype.

Mutant phenotypes = Phenotypes that are alternatives ti the wild type and which are due to mutations in the wild-type gene.

B. Discovery of a Sex-Linked Gene

After a year of breeding Drosophila to find variant phenotypes, Morgan discovered a single male fly with white eyes instead if the wild-type red. Morgan mated this mutant white-eyed male with a red-eyed female. The cross is outlined below.

w = white-eyed allele Drosophila geneticists symbolize a recessive

w⁺= red-eyed or wild-type allele

Morgan deduced that eye color is linked to sex ab that the gene for wye color is located only on the X chromosome. Premises for his conclusions were

Ø If eye color is located only on the X chromosome, then females (XX) carry two copies of the gene, while males (XY) have only one.

Ø Since the mutant allele is recessive, a white-eyed female must have that allele on both X chromosomes which was impossible for F₂ females in Morgan’s experiment.

Ø A white-eyed males has no wild-type allele to mask the recessive mutant allele, so a single copy of the mutant allele confers white eyes.

Sex-linked genes = Genes on sex chromosomes. The term is commonly applies only to genes on the X chromosome, but does include those on Y also.

III. Linked genes tend to be inherited together because they are located on the same chromosome

Genes located on the same chromosome tend to be linked in inheritance and od not assort independently.

Linked genes = Genes that are located on the same chromosome and that tend to be inherited together

Ø Linked genes do not assort independently, because they are on the same chromosome and move together through meiosis and fertlization.

Ø Since independent assortment does not occur, a dihybrid cross following to linked genes will not produced an F₂ phenotypic ratio of 9:3:3:1.

T.H. Morgan and his students performed a dihybrid testcross between flies with autosomal recessive mutant alleles for balck bodies and vestigial wings and wild-type flies heterozygous for both traits. (A more detailed description follows in a later section.)

b = black body vg = vestigial wings

b⁺= gray body vg⁺= wild-type wings

b⁺bvg⁺vg x bbvgvg

gray, normal wings black, vestigial wings

Ø Resulting phenotypes of the progeny did not occur in the expected 1:1:1:1 ration for a dihybrid testcross.

Ø A disproportionately large number of flies had the phenotypes of the parents: gray with normal wings and black with vestigial wings.

Ø Morgan proposed that these unusual ratios were due to linkage. The genes for body color and wing size are in the same chromosome and are usually thus inherited together.

IV. Independent assortment of chromosome and crossing over genetic recombination

Genetic recombination = The production of offspring with new combination of traits different from those combinations found in the parents; results from the events of meiosis and random fertilization.

A. The Recombination of Unliked Genes: Independent Assortment of Chromosomes

Mendel discovered that some offspring from dihybrid crosses have phenotypes unlike either parent. An example is the following test cross between pea plants:

YY, Yy = yellow seeds RR, Rr = round seeds

yy = green seeds rr = wrinkled seeds

P generation:

YyRr X yyrr

yellow round green wrinkled

Testcross Progeny:

¼ YyRr

Parental types = Progeny that have the same phenotype as one or the other of the parents.

Recombinants = Progeny wgose phenotypes differ from wither parent.

In this cross, seed shape and seed color are unlinked.

Ø One-fourth of the progeny have round yellow seeds, and one fourth have wrinkled green seeds. Therefore, one-half of the progeny are parental types.

Ø The remaining half of the progeny are recombinants. One fourth are round green and one fourth are wrinkled yellow – phenotypes not found in either parent.

Ø When half the progeny are recombinants, ther is a 50% frequency of recombination.

Ø A 50% frequency of recombination usually indicates that the two genes are on different chromosomes, because it is the expected result if the two genes assort randomly.

Ø The genes for seed shape and seed color assort independently of one another because they are located on different chromosomes which randomly align during metaphase of meiosis I.

B. The Recombination of Linked Genes: Crossing Over

If genes are totally linked, some possible phenotypic combinations should not appear. Sometimes, however, the unexpected recombinant phenotypes do appear.

As described earlier, T.H. Morgan and his students performed the following dihybrid testcross betweem flies with autosomal recessive mutant alleles for black bodies and vestigial wings and wild-type flies heterozygous for both traits.

b = black body vg = vestigial wings

b⁺= gray body vg⁺ = wild-type wings

b⁺bvg⁺vg X bbvgvg

gray, normal wings black, vestigial wings

Phenotypes	Genotypes	Expected Results If Genes Are Unlinked	Expected Results If Gtenes Are Totally Linked	Actual Results
Black body, normal wings	b vg⁺ b vg	575	-	206
Gray body, normal wings	b⁺vg⁺ b vg	575	1150	965
Black body, vestigial wings	b vg b vg	575	1150	944
Gray body, vestigial wings	b⁺vg b vg	575	-	185

Recombination Frequency = 391 recombinats X 100 = 17%

2300 total offspring

Morgan’s results from this dihybrid testcross showed that the two genes were neither unlinked nor totally linked.

Ø If wing type and body color genes were unlinked, they would assort independently, and the progeny would show a 1:1:1:1 ratio of all possible phenotypic combinations.

Ø If genes were completely linked, expected results from the testcross would be a 1:1 phenotyic ratio of parental types only.

Ø Morgan’s testcross did not produce results consistent with unlinkage or total linkage. The high proportion of parental phenotypes suggested linkage between the two genes.

Ø Since 17% of the progeny were recombinants, the linkage must be incomplete. Morgan proposed that there must be some mechanism that occasionally breaks the linkage between the two genes.

Ø It is now known that crossing over during meiosis accounts for the recombination of linked genes. The exchange of parts between homologous chromosomes breaks linkages in parental chromosomes and forms recombinants with new allelic combinations.

V. Genetics can use recombination data to map a chromosome’s genetic loci

Scientists used recombination frequencies between genes to map the sequence of linked genes on particular chromosomes.

Morgan’s Drosophila studies showed that some genes are linked more tightly than others.

Ø For example, the recombination frequency between the b and vg loci is about 17%.

Ø The recombination frequency is only 9% between b and cn, a third locus on the same chromosome. (The cinnabar gene, cn, for eye color has a recessive allele causing “cinnabar eyes.”)

A.H. Sturtevant, one of Morgan’s students, assumed that if crossing over occurs randomly, the probability of crossing over between two genes is directly proportional to the distance between them.

Ø Sturtevant used recombination frequencies between genes to assign them a linear position on a chromosome map.

Ø He defined one map unit as 1% recombination frequency. (Map units are now called centimorgans, in honor of Morgan.)

Using crossover data, a map may be constructed as follows:

Loci	Recombination Frequency	Approximate Map Units
b vg	17.0	18.5
cn b	9.0%	9.0
cn vg	9.5%	9.5

Establish the relative distance between those genes farthest apart or with the highest recombination frequency.

b vg

2. Determine the recombination frequency between the third gene (cn) and the first (b).

cn b

3. Consider the two possible placements of the third gene:

4. Determine the recombinant frequency between the third gene (cn) and the second (vg) to eliminate the incorrect sequence:

So, the correct sequence is b-cn-vg.

*Note that there are actually 18.5 map units between b and vg. This is higher than that predicted from the recombination frequency of 17.0% Because b and vg are relatively far apart, double crossovers occur between these loci and cancel each other out, leading us to underestimate the actual map.

If linked genes are so far apart on a chromosome that the recombination frequency is 50%, they are indistinguishable from unlinked genes that assort independently.

Ø Linked genes that are far aprat can be mapped, if additional recombination frequencies can be determined between intermediate genes and each of the distant genes.

Sturtevant and his coworkers extended this method to map other Drosophila genes in linear arrays.

Ø The crossover data allowed them to cluster the known mutations into four major linkage groups.

Ø Since Drosophila has four sets of chromosomes, this clustering of genes into four linkage groups was further evidence that genes are on chromosomes.

Map based on crossover data only give information about the relative position of linked genes on a chromosome. Another technique, cytological mapping pinpoints the actual location of genes and the real distance between them.

Ø Cytological mapping involves screening offspring for mutant phenotypes and associating mutants with chromosomal defects visible by direct microscopic examination.

Ø The location of loci derived from maps based in crossover data differs from the spacing derived from cytological mapping, because the frequency of crossing over is not the same for all chromosomal regions.

VI. The chromosomal basis of sex produces unique patterns of inheritance

In most species, sex is determined by the presence or absence of special chromosomes. As a result of meiotic segregation, each gamete has one sex chromosome to contribute at fertilization.

Heterogametic sex = The sex that produces two kinds of gametes and determines the sex of the offspring. (XY)

Homogametic sex = The sex that produces one kind of gamete.(XX)

A. The Chromosomal Basis of Sex in Humans

Mammals, including humans, have an X-Y mechanism that determines sex at fertilization.

Ø There are two chromosomes, X and Y. Each gamete has one sex chromosome, so when sperm cell and ovum unite at fertilization, the zygote receives one of the two possible combinations: XX or XY.

Ø Males are the heterogametic sex (XY). Half the sperm cells contain an X chromosome, while the other half contain a Y chromosome.

Ø Females are the homogametic sex (XX); all ova carry an X chromosome.

Whether an embryo develops into a male or female depends upon the presence of a Y chromosme.

Ø A British research team has identified a single gene, Sry (sex-determining region), on the Y chromosome that is responsible for triggering the complex series of events that lead to normal testicular development.

Ø Sry probably codes for a protein that regulates other genes.

B. Sex-Linked Disorders in Humans

Some genes on sex chromosomes play a role in sex determination, but these chromosomes also contain genes for other traits.

In humans, the term sex-linked traits usually refers to X-linked traits.

Ø The human X-chromosome is much larger than the Y. Thus, there are more X-linked than Y-linked traits.

Ø Most X-linked genes have no homologous loci on the Y chromosome.

Ø Most genes on the Y chromosome not only have no counterparts, but they encode traits found only in males (e.g. testis-determining factor).

Fathers pass X-linked alleles to only and all of their daughters.

Ø Males receive their X chromosme only from their mothers.

Ø Fathers cannot, thereforem pass sex-linked traits to their sons.

Mothers can pass sex-linked alleles to both sons and daughtes.

Ø Females receive two X chromosomes, one form each parent.

Ø Mothers pass on one X chromosome (either maternal or paternal homologue) to every daughter and son.

If a sex-linked trait is due to a recessive allele, a female will express the trait if she is homozygous.

Ø Females have two X chromosomes, therefore they can be either homozygous or heterozygous for sex-linked alleles.

Ø There are fewer females with sex-linked disorders than males, because even if they have one recessive allele , the other dominant allele is the one that is expressed. A female that is heterozygous for the trait can be a carrier, but not show the recessive trait herself.

Ø A carrier that mates with a normal male will pass the mutation to half her sons and half her daughters.

Ø If a carrier mates with a male who has the trait, there is a 50% chance that each child born to them will have the trait, regardless of sex.

Because males have only one X-linked locus, any male receiving a mutant allele from his mother will express the trait.

Ø Far more males than females have sex-linked disorders.

Ø Males are said to hemizygous.

Hemizygous – A condition where only one copy of a gene is present in a diploid organism.

C. X-Inactivation in Females

How does an organism compensate for the fact that some individual have a double dosage of sex-linked genes while others have only one?

In female mammals, most diploid cells have only one fully functional X chromosome.

Ø The explanation for this process is known as the Lyon hypothesis, proposed by the British geneticist Mary F. Lyon.

Ø In females, each of the embryonic cells inactivates one of the two X chromosomes.

Ø The inactive X chromosome contracts into a dense object called a Barr body.

Barr body = Inside the nuclear envelope, a densely staining object that is an inactivated X chromosome in female mammalian cells.

Ø Most Barr body genes are not express.

Ø Are reactivated in gonadal cells that undergo meiosis to form gametes.

Females mammals are a mosaic of two types of cells- those with an active maternal X and those with an active paternal X.

Ø Which of the two Xs will be inactivated is determined randomly in embryonic cells.

Ø After an X is inactivated, all mitotic descendant will have the same inactive X.

Ø As a consequence, if a female is heterozygous for a sex-linked trait, about half of her cells will express one allele and the other cells well express the alternate allele.

Ø Examples of this type of mosaicism are coloration in calico cats ad normal sweat gland development in humans.

X chromosome inactivation is associated with DNA methylation.

· Methyl groups (-CH₃) attach to cytosine, one of DNA’s nitrogenous bases.

· Barr bodies are highly methylated compared to actively transcribed DNA.

What determines which of the two X chromosomes will be methylated?

· A recently discovered gene, XIST is active only of the Barr body.

· The product of the XIST gene, X-inactive specific transcript, is an RNA that interacts with the X chromosome and maintains its inactivation.

VII. Alteration of chromosome number or structute cause some genetic disorders

Nondisjunction = Meiotic or mitotic error during which certain homologous chromosomes or sister chromatids fail to separate.

· Meiotic nondisjunction:

Ø May occur during Meiosis I so that homologous pair does not separate.

Ø May occur during Meiosis II when sister chromatids do not separate.

Ø Results in one gamete receiving two of the same typw of chromosome ans another gamete receiving no copy. The remaining chromosomes may be distributed normally.

· Mitotic nondisjunction:

Ø Also results in abnormal number of certain chromosomes.

Ø If it occurs in embryonic cells, mitotic division passes this abnormal chromosome number to a large number of cells, and thus have a large effect.

Aneuploidy = Condition of having an abnormal number of certain chromosomes.

· Triploidy is a polyploid chromosome number with three haploid chromosome sets (3N).

· Tetraploidy is a polyploidy with four haploid chromosmes sets (4N).

· Triploids may result if a diplors zygote undergoes mitosis without cytokinesis. Subsequent normal mitosis weould produce a 4N embryo.

· Polyploidy is common in plants and important in plant evoltion.

· Polyploids occur rarely among animals, and they are more normal in appearance than aneuploids. Mosaic polyploids, with only patches of polyploid cells, are more common than complete plyploid animals.

B. Alterations of Chromosome Structure

Chromosome breakage can alter structure in four ways:

· Chromosomes which lose a fragment lacking a centromere will have a defiency or deletion.

· Fragments without centromeres are usually lost when the cell divides, or theu may:

Ø Join to a homologous chromosome producing a duplication.

Ø Join to a nonhomologous chromosome (translocation).

Ø Reattach to the origianl chromosome in reverse order (inversion).

Crossing-over error is another source of deletions and duplications.

· Crossovers are normally reciprocal, but sometimes one sister chromatid gives up more than it receives in an unequal crossover.

· A nonreciprocal crossover results in one chromosome with a deletion and one chromosome with a duplication.

Alteration of chromosme structure, can have various effects:

· Homozygous deletions, including a single X in a male, are usually lethal.

· Duplication and translocations tend to have deleterious effects.

· Even if all genes are present in normal dosages, reciprocal translocations between nonhomologous chromosmes and inversions can alter the phenotype because of subtle position effects.

Position effect = Influence on a gene’s expression because of its location among neighboring genes.

C. Human Disorders Due to Chromosomal Alterations

Chromosomal alteration are associated with some serious human disorders.

Aneuploidy, resulting from meiotic nondisjunction during gamete formation, usually prevents normal embryonic developmet and often results in spontaneous abortion.

· Some types of aneuploidy cause less severe problems, and aneuploid individuals may survive to birth and beyond with a set of characteristic symptoms or syndrome.

· Aneuploid conditions can be diagnosed before birth by fetal testing.

Down syndrome, and aneuploid condition, affects 1 out of 700 U.S. children.

· Is usually the result or trisomy 21

· Includes characteristc facial features, short stature, heart defects, mental retardation, susceptibility to respiratory infections, and a proneness to developing leukemia and Alzhemimer’s disease.

· Through most are sexually underdeveloped and sterile, a few women with Down syndrome have had children.

· The incidence of Down syndrome offspring correlates with maternal age.

Ø May be related to the long time lag between the first meiotic division during the mother’s fetal life and the completion of meiosis at ovulation.

Ø May be that older women have less chance of miscarrying a trisomic embryo.

Other rarer disorders caused by autosomal aneuploidy are:

· Patau syndrome (trisomy 13)

· Edwards syndrome (trisomy 18).

Sex chromosomes aneuploidies result in less severe conditions than those from autosomal aneuploidies. This may be because:

· The Y chromosome carries few genes.

· Copies of the X chromosome become inactivated as Barr bodies.

The basis of sex determination in humans is illustrated by sex chromosome aneuploidies.

· A single Y chromosome is sufficient to produce maleness.

· The absence of Y is required for femalesness.

Examples of sex chromosome aneuploidy in males are:

Klinefelter Syndrome

Genotype: Usually XXY, but may be associated with XXYY, XXXY, XXXXY, XXXXXY.

Phenotype: Male sex organs with abnormally small testes; sterile; femine body contours and perhaps breast enlargement; usually of normal intelligence.

Extra Y

Genotype: XYY.

Phenotype: Normal male; usually taller than average; normal intelligence and fertility.

Abnormalities of sex chromosome number in females include:

Triple-X Syndrome

Genotype: XXX.

Phenotype: Usually fertile; can show a normal phenotype.

Turner Syndrome

Genotype: XO (only known viable human monosomy).

Phenotype: Short stature; at puberty, secondary sexual characteristics fail to develop; internal sex organs do not mature; sterile.

Structural chromosomal alterations such as deletions and translocations can also cause human disorders.

Ÿ Deletions in human chromosome cause severe defects even in the heterozygous state. For example,

Þ Cri du chat syndrome is caused by a deletion on chromosome 5. Symptoms are mental retardation, a small head with unusual facial features and a cry that sounds like a mewing cat.

Ÿ Translocations associated with human disorders include:

Þ Certain cancers such as chronic myelogenous leukemia (CML). A portion of chromosome 22 swirches places with a small fragment from chromosome 9.

Ÿ Some cases of Down syndrome. A third chromosome 21 translocates to chromosome 15, resulting in two normal chromosome 21 plus the translocation.

VIII. The phenotypic effects of some genes depend on whether they were inherited from the mother or father.

A. Genomic Imprinting

The expression of some traits may depend upon which parent contributes the alleles for syndrome, are caused by the same deletion on chromosome 15. The symptoms differ depending upon whether the gene was inherited from the mother or from the father.

Ÿ For example, two genetic disorders, Prader-Willi syndrome and Angelman syndrome, caused by the same deletion on chromosome 15. The symptoms differ depending upon whether the gene was inherited from the mother or from the father.

Ÿ Prader-Willi syndrome is caused by a deletion from the paternal version of chromosome 15. The syndrome is characterized by mental retardation, obesity, short stature, and unusually small hands and feet.

Ÿ Angelman syndrome is caused by a deletion from the maternal version of chromosome 15. This syndrome is characterized by uncontrolled spontaneous laughter, jerky movements, and other motor and mental symptoms.

Ÿ The Prader-Willi/Angelman syndromes imply that the deleted genes normally behave a differently in offspring, depending on whether they belong to the maternal or the paternal homologue.

Ÿ In other words, homologous chromosomes inherited from males and females are somehow differently imprinted, which causes them to be functionally different in the offspring.

Genomic imprinting = Process that induces intrinsic changes in chromosome inherited from males and females; caused certain genes to be differently expressed in the offspring depending upon whether the alleles were inherited from the ovum or from the sperm cell.

Ÿ According to this hypothesis, certain genes are imprinted in some way each generation, and the imprint is different depending on whether the genes reside in females or in males.

Ÿ The same alleles may have different effects on offspring depending on whether the genes reside in females or in males.

Ÿ The same allele may have different effects on offspring depending on whether they are inherited from the mother or the father.

Ÿ In the new generation, both maternal and paternal imprints can be reversed in gamete-producing cells, and all the chromosome are re-coded according to the sex of the individual in which they now reside.

Ÿ DNA methylation may be one mechanism for genomic imprinting.

B. Fragile-X and Triplet Repeats

Triplet repeats = Sections of DNA where a specific triplet of nucleotides is repeated many times.

Ÿ Occur normally in many places within the human genome.

Ÿ Progressive addition of triplet repeats can lead to genetic disorders such as Fragile-X syndrome and Huntington’s disease.

Affecting about one in every 1500 males and one in every 2500 females, Fragile-X syndrome is the most common genetic cause of mental retardation.

Ÿ The “fragile X” is an abnormal X chromosome, the tip of which hangs on the rest of the chromosome by a thin DNA thread. This altered region in fragile-X, as well as the comparable region in normal X chromosomes, contains triplet repeats.

Ÿ The triplet repeat, CGG (cytosine, guanine, guanine), is repeated up to 50 times in one tip of a normal X chromosome, but is repeated more than 200 times in a fragile X chromosome.

Ÿ Abnormal addition of triplet repeats occurs incrementally over generations, so there is a “prefragile-X” condition between 50 to 200 CGG repeats; these individuals are phenotypically normal. Eventually, as enough repeats accrue from one generation to the next, fragile-X syndrome appears.

Fragile-X syndrome’s complex expression may be a consequence of maternal genomic imprinting.

Ÿ The syndrome is more likely to appear if the abnormal X chromosome is inherited from the mother rather than the father, and pre-fragile X chromosomes in ova producing cells more likely to acquire new CGG triplets than chromosomes in sperm producing cells.

Ÿ In the female parent, the site of triplet repeats on the X chromosome is imprinted by DNA methylation. Excessive methylation may inactivate one or more genes and prevent their normal expression in offspring.

Ÿ Maternal imprinting explains why fragile-X disorder is more common in males. Males (XY) inherit the fragile X chromosome only from their mothers - maternally imprinted versions of the abnormal chromosome.

Ÿ Females can inherit the fragile X chromosome from either parent, but only the maternal version is imprinted and caused expression of the syndrome. Heterozygous carriers for this recessively inherited trait, have partial protection from the normal X chromosome and are usually only mildly retarded.

Huntington’s disease is another example of how extended triplet repeats and genomic imprinting can influence the expression of human genetic disorder.

Ÿ The Huntington’s locus, near the tip of chromosome #4, has a CAG extended triplet repeat.

Ÿ Genomic imprinting influences the expression of the gene. The triplet repeat at the Huntington’s locus is more likely to extend if the allele is inherited from the father, rather than the mother.

IX. Extranuclear genes exhibit a non-mendelian pattern of inheritance

There are some exceptions to the chromosome theory of inheritance.

Ÿ Extranuclear genes are found in cytoplasm organelles such as plastids and mitochondria.

Ÿ These cytoplasm genes are not inherited in Mendelian fashion, because they are not distributed by segregating chromosomes during meiosis.

In plants, a zygote receives its plastids from the ovum, not from pollen. Consequently, offspring receive only maternal cytoplasm genes.

Ÿ Cytoplasmic genes in plants were first described by Karl Corens (1909) when he noticed that plant coloration of an ornamental species was determined by the seed bearing plants and not by the pollen producing plants.

Ÿ It is now known that maternal plastid genes control variegation of leaves.

In mammals, inheritance of mitochondria DNA is also exclusively maternal.

Ÿ Since the ovum contributes most of the cytoplasm to the zygote, the mitochondria are all maternal in origin.