EXTRACHROMOSOMAL INHERITANCE
Cytoplasmic, Organelle and Maternal Inheritance (Non-Mendelian Inheritance)
Prepared by
Dr Bhabesh Nath
Assistant Professor
Department of Zoology
B N College, Autonomous Dhubri
1. Introduction
According to Mendel's laws, hereditary traits are controlled by genes located on nuclear chromosomes, which are distributed to offspring equally through the egg and the sperm. However, some traits are passed on through genetic material that lies outside the nucleus, in the cytoplasm. This phenomenon is called extrachromosomal (extranuclear, cytoplasmic or non-Mendelian) inheritance. The genes concerned are carried on organelle DNA (mitochondria and plastids), on plasmids, or on the DNA or RNA of endosymbionts and viruses living in the cytoplasm.
The first clear cases were reported in 1909 by Carl Correns in the four-o'clock plant Mirabilis jalapa and by Erwin Baur in Pelargonium zonale, both involving variegated (green and white) leaves. Because the egg contributes nearly all of the cytoplasm of the zygote while the sperm contributes almost none, extrachromosomal inheritance is usually uniparental and maternal.
1.1 Criteria for recognising extrachromosomal inheritance
• Reciprocal crosses give different results; the phenotype of the progeny follows the female parent (maternal inheritance), not both parents equally.
• No Mendelian segregation ratios (such as 3:1 or 9:3:3:1) are seen in the F2 or in the progeny of backcrosses.
• The trait is not linked to any nuclear gene and its transmission is not affected by replacing the nucleus by repeated backcrossing (the cytoplasmic trait persists).
• The trait is often associated with a cytoplasmic particle (organelle DNA, plasmid or symbiont) that can be identified, and may be transferred by cytoplasmic transfer or infection.
1.2 Differences between nuclear and extranuclear inheritance
Feature | Nuclear (Mendelian) inheritance | Extranuclear inheritance |
Location of genes | Chromosomes in the nucleus | Mitochondria, plastids, plasmids, cytoplasmic symbionts |
Contribution of parents | Equal from both parents | Mainly or only from one parent, usually the mother |
Reciprocal crosses | Give the same result | Give different results |
Segregation | Regular, at meiosis (Mendelian ratios) | Irregular, random sorting of organelles at cell division; no Mendelian ratios |
Gene linkage | Genes show linkage and can be mapped | Not linked to nuclear genes |
Effect of nuclear substitution | Trait changes with the nucleus | Trait persists after nuclear replacement |
Number of gene copies | Two per cell (diploid) | Many copies per cell (many organelles) |
2. Origin of Organelle Genomes: The Endosymbiotic Theory
Mitochondria and chloroplasts have their own DNA, ribosomes and protein-synthesis machinery because they evolved from free-living bacteria engulfed by an ancestral eukaryotic cell (Mereschkowsky 1905; revived by Lynn Margulis, 1967). Mitochondria are derived from α-proteobacteria and chloroplasts from cyanobacteria. Evidence includes:
• Circular, histone-free DNA like that of bacteria, and 70S ribosomes sensitive to antibiotics such as chloramphenicol.
• Double membranes, replication by binary fission, and bacterial-type RNA polymerase and gene organisation.
• Gene transfer to the nucleus over evolutionary time: most organelle proteins (over 95% in mitochondria) are encoded by nuclear genes and imported, so organelles are semi-autonomous.
3. Plastid (Chloroplast) Inheritance
3.1 Plastid genome
• Circular DNA of about 120–160 kb in most land plants (tobacco 155,844 bp, completely sequenced by Shinozaki et al. in 1986); present in many copies per plastid and many plastids per cell.
• Encodes rRNAs, tRNAs, ribosomal proteins, subunits of RNA polymerase, photosystem I and II proteins, ATP synthase subunits and the large subunit of RuBisCO (rbcL). The small subunit of RuBisCO is nuclear-encoded.
3.2 Variegation in Mirabilis jalapa (Correns, 1909)
Plants of Mirabilis jalapa have branches with green, white (colourless, lacking chlorophyll) or variegated (mosaic) leaves. Correns pollinated flowers on each type of branch with pollen from another branch type and observed that the seedlings always resembled the branch bearing the female flower (seed parent), irrespective of the pollen source.
Seed parent (♀ branch) | Pollen parent (♂ branch) | Progeny |
Green | Green, white or variegated | All green |
White | Green, white or variegated | All white (seedlings die because they lack chlorophyll) |
Variegated | Green, white or variegated | Green, white and variegated seedlings in varying proportions |
Explanation: the egg cytoplasm carries the plastids; the pollen contributes almost none. Green branches have normal chloroplasts, white branches have defective plastids (a mutation in plastid DNA), and variegated branches contain both types in the same cell. During cell division the two types of plastids are sorted out randomly (vegetative segregation), producing green, white and mixed cells. Eggs from variegated branches may therefore contain only normal plastids, only mutant plastids, or both.
3.3 Other examples and exceptions
• Pelargonium zonale (Baur, 1909): both parents contribute plastids (biparental inheritance), so reciprocal crosses give mixed progeny; Baur proposed that plastids have their own hereditary determinants.
• Oenothera (evening primrose): plastid types (plastomes I–V) show biparental transmission and incompatibility with certain nuclear genomes (genome–plastome incompatibility), studied by Renner and Stubbe.
• Gymnosperms (e.g. pines) show paternal plastid inheritance; most angiosperms are maternal, and some are biparental.
• Chlamydomonas reinhardtii (Sager, 1954): an alga with two mating types, mt⁺ and mt⁻. Streptomycin resistance determined by a chloroplast gene was transmitted only from the mt⁺ parent (uniparental inheritance, the chloroplast DNA of mt⁻ is degraded after zygote formation), whereas a nuclear gene for resistance showed a Mendelian 1:1 segregation.
4. Mitochondrial Inheritance
4.1 Human mitochondrial genome
Feature | Description |
Size and form | 16,569 bp, circular, double-stranded, with a heavy (H) and a light (L) strand; sequenced by Anderson et al., 1981 (Cambridge reference sequence) |
Gene content | 37 genes: 13 polypeptides (subunits of complexes I, III, IV and ATP synthase), 22 tRNAs and 2 rRNAs |
Organisation | Compact, almost no introns or intergenic spacers; the non-coding D-loop (control region) holds the origin of H-strand replication and promoters; transcribed as polycistronic units |
Copy number | Several thousand copies per somatic cell (2–10 per mitochondrion); over 100,000 in the mature oocyte |
Features | Not wrapped in histones, limited repair, mutation rate 10–20× higher than nuclear DNA; modified genetic code |
Variant codons | UGA = Trp (not stop), AUA = Met (not Ile), AGA and AGG = stop (not Arg) |
4.2 Maternal inheritance
The oocyte provides almost all of the mitochondria of the zygote. The few mitochondria of the sperm (in the midpiece) are tagged with ubiquitin and destroyed inside the egg (Sutovsky et al., 1999), so mtDNA is transmitted through the mother to all her children, but only her daughters pass it on. Rare reports of paternal leakage in humans exist but remain controversial.
Figure 1. Pedigree of a mitochondrial disorder: an affected mother passes the trait to all her children, an affected father to none.
4.3 Heteroplasmy, segregation and the threshold effect
• A cell may carry both normal and mutant mtDNA, a condition called heteroplasmy (when all copies are identical it is homoplasmy).
• During cell division mitochondria are distributed randomly to daughter cells (replicative and mitotic segregation), so the proportion of mutant mtDNA drifts and differs between tissues.
• A bottleneck in the female germline (a small number of mtDNA copies populate the primary oocytes) causes the proportion of mutant mtDNA to vary greatly between siblings.
• Disease appears only when the proportion of mutant mtDNA exceeds a threshold (often 60–90%), and tissues with high energy demand (brain, heart, muscle, retina, kidney) are affected first.
4.4 Human mitochondrial diseases
Disease | Mutation | Main features |
LHON (Leber hereditary optic neuropathy) | Point mutations, e.g. G11778A in ND4 (Wallace et al., 1988) | Sudden loss of central vision in young adults, more frequent in males |
MERRF | A8344G in tRNA-Lys | Myoclonic epilepsy with ragged-red muscle fibres, ataxia, deafness |
MELAS | A3243G in tRNA-Leu(UUR) | Mitochondrial encephalopathy, lactic acidosis, stroke-like episodes |
Kearns–Sayre syndrome | Large mtDNA deletion (usually sporadic) | Ophthalmoplegia, retinal degeneration, heart block |
NARP / Leigh syndrome | T8993G in ATP6 | Neuropathy, ataxia, retinitis pigmentosa; severe infantile encephalopathy |
Mitochondrial DNA is also used to trace maternal lineages (mitochondrial 'Eve'), in population studies, in forensic identification (for example identification of the remains of the Romanov family) and in studying ancient DNA. Mitochondrial replacement therapy (pronuclear or spindle transfer, 'three-parent baby') has been developed to prevent transmission of severe mtDNA diseases and is regulated in countries such as the UK and Australia.
4.5 Yeast petite mutants (Ephrussi, 1949)
Saccharomyces cerevisiae forms small (petite) colonies when it lacks functional mitochondria and cannot respire, so it grows only by fermentation. Three types are recognised:
Type | Nature | Result in a cross with wild type |
Segregational petite | Nuclear gene mutation | Mendelian 2:2 segregation of normal and petite spores |
Neutral petite (ρ⁻/ρ⁰) | Large deletion or loss of mtDNA | Diploid is normal, and all four spores of every tetrad are normal (4:0, non-Mendelian) |
Suppressive petite | Partly deleted mtDNA that out-competes normal mtDNA | Diploid and a large fraction of progeny are petite |
4.6 Poky in Neurospora (Mitchell and Mitchell, 1952)
The poky strain of Neurospora crassa grows slowly and lacks normal cytochromes because of a mitochondrial DNA mutation. In crosses, poky is transmitted only through the protoperithecial (female) parent, whichever strain acts as the male gives no effect, which demonstrates maternal inheritance.
5. Cytoplasmic Male Sterility (CMS) in Plants
• CMS is the inability to produce functional pollen while female fertility is normal. It is determined by a mitochondrial gene (an abnormal chimeric open reading frame, for example T-urf13 in maize cms-T) and inherited maternally.
• Fertility can be restored by dominant nuclear restorer-of-fertility (Rf) genes. Genotype notation: S(rfrf) = male sterile; N(rfrf), N(RfRf) and S(RfRf) = male fertile (N = normal cytoplasm, S = sterile cytoplasm).
• CMS is used to produce hybrid seeds without laborious manual emasculation in maize, sorghum, pearl millet, rice, sunflower and onion (A line = male sterile, B line = maintainer, R line = restorer).
• Maize T-cytoplasm was also sensitive to the fungus Helminthosporium maydis race T, and widespread use of it led to the Southern corn leaf blight epidemic in the USA in 1970, illustrating the risk of genetic uniformity.
6. Infective Heredity: Cytoplasmic Symbionts and Viruses
6.1 Kappa particles and killer paramecia (Sonneborn, 1943)
• Paramecium aurelia strains are of two kinds: killer strains that secrete a toxin (paramecin) killing sensitive strains, and sensitive strains.
• Killing depends on cytoplasmic particles called kappa, which are intracellular bacteria (Caedibacter taeniospiralis); particles with refractile (R) bodies release the toxin.
• Kappa can be maintained only in the presence of a dominant nuclear gene K: KK or Kk cells can be killers, kk cells lose kappa and become sensitive. Thus the trait needs both a nuclear gene and a cytoplasmic particle.
• In conjugation without cytoplasmic exchange, the partners keep their phenotypes. If conjugation is prolonged so that cytoplasm mixes, kappa passes into the sensitive cell and converts it into a killer, showing that kappa is cytoplasmic.
6.2 CO₂ sensitivity in Drosophila
Some Drosophila are killed by exposure to CO₂ (normal flies are only anaesthetised). The sensitivity is caused by the sigma virus (a rhabdovirus), transmitted through the egg cytoplasm (L'Héritier and Teissier, 1937); it is therefore maternally inherited, although it can also be transmitted through sperm at a lower frequency.
6.3 Wolbachia
Wolbachia are endosymbiotic bacteria in the cytoplasm of many insects, transmitted through the egg. They manipulate the host's reproduction by cytoplasmic incompatibility (infected males mated to uninfected females give no viable offspring), male killing, feminisation and parthenogenesis induction. Wolbachia-infected Aedes aegypti mosquitoes are now used to reduce dengue transmission.
6.4 Other examples
• Milk factor in mice (Bittner): the mouse mammary tumour virus is transmitted through milk and causes mammary cancer in susceptible strains.
• Yeast prions: [PSI⁺] (Sup35 protein) and [URE3] (Ure2 protein; Wickner, 1994) are self-propagating protein conformations that are inherited through the cytoplasm, a protein-based, non-DNA inheritance.
7. Plasmids as Extrachromosomal Elements
Plasmids are autonomously replicating, usually circular DNA molecules found in bacteria and some yeasts. An episome (Jacob and Wollman, 1958) is a plasmid that can also integrate into the chromosome.
Plasmid | Characters |
F (fertility) factor | About 100 kb; carries tra genes for conjugation and pilus formation; integrates to make Hfr strains |
R (resistance) plasmids | Carry genes for antibiotic resistance (R-determinants) and RTF (resistance transfer factor); spread resistance between bacteria |
Col plasmids | Encode colicins (bacteriocins) that kill related bacteria |
Degradative plasmids | Encode enzymes to break down toluene, camphor and other compounds (e.g. Pseudomonas) |
Ti plasmid | Of Agrobacterium tumefaciens; transfers T-DNA to plant cells to cause crown gall; used in plant genetic engineering |
2 µm plasmid | Of yeast; used in yeast cloning vectors |
8. Maternal Effect (Predetermination) – Not True Extrachromosomal Inheritance
In a maternal effect, the phenotype of an offspring is determined by the nuclear genotype of the mother, not by its own genotype, because gene products (mRNA and proteins) deposited in the egg cytoplasm control early development. The genes are chromosomal and obey Mendelian segregation, but the effect appears one generation late (delayed Mendelian inheritance), so it mimics cytoplasmic inheritance.
8.1 Shell coiling in the snail Limnaea peregra
• The direction of shell coiling is either dextral (right-handed, allele D) or sinistral (left-handed, allele d); D is dominant. It is determined by the orientation of the spindle at the first cleavage of the egg, which is set by the mother's genotype (Sturtevant, 1923; Boycott and Diver).
• Cross: sinistral (dd) ♀ × dextral (DD) ♂ → F1 (Dd) are all sinistral (mother is dd). F1 self-fertilised → F2 genotypes 1 DD : 2 Dd : 1 dd but all dextral (the F1 mother is Dd). F2 self-fertilised → F3 shows 3 dextral : 1 sinistral, as dd mothers produce sinistral offspring.
8.2 Other examples
• Ephestia kuehniella (flour moth): the dominant allele A gives enzymes for kynurenine synthesis, needed for dark eye pigment. Larvae of genotype aa from Aa mothers have normal pigmentation as the egg contains the maternal substance, but lose it as the larva grows (Kühn).
• Drosophila embryo: bicoid and nanos mRNAs deposited by the mother set up the anterior–posterior axis, and dorsal the dorsoventral axis; embryos from mutant mothers fail to develop correctly (maternal-effect genes).
8.3 Maternal effect compared with cytoplasmic inheritance
Feature | Maternal effect | Cytoplasmic (organelle) inheritance |
Genes involved | Nuclear (chromosomal) genes of the mother | Genes of mitochondria, plastids, plasmids or symbionts |
Segregation | Mendelian but delayed by one generation | No Mendelian segregation |
Persistence | Effect lasts one generation | Persists over generations through the female line |
Example | Limnaea coiling, Ephestia | Mirabilis variegation, human LHON |
9. Quick Summary
• Extrachromosomal inheritance is due to genes outside the nucleus; it is usually maternal and shows non-Mendelian ratios and differences in reciprocal crosses.
• Plastid inheritance: Mirabilis (maternal), Pelargonium (biparental), Chlamydomonas (mt⁺ uniparental). Mitochondrial: human mtDNA 16,569 bp, 37 genes, heteroplasmy, LHON, MERRF, MELAS; yeast petites; Neurospora poky.
• CMS in plants is mitochondrial and is restored by nuclear Rf genes. Infective heredity: kappa in Paramecium, sigma virus, Wolbachia. Plasmids: F, R, Col.
• Maternal effect (Limnaea coiling) is determined by the mother's nuclear genotype and is delayed Mendelian inheritance.
10. Multiple Choice Questions (10)
Q1. Who first reported extranuclear inheritance of leaf variegation in Mirabilis jalapa in 1909?
(a) Mendel
(b) Correns
(c) Morgan
(d) Sonneborn
Q2. In Mirabilis jalapa, seeds produced on a white branch pollinated by pollen from a green branch give:
(a) All green seedlings
(b) All white seedlings
(c) Variegated seedlings
(d) Green and white in 1:1 ratio
Q3. The human mitochondrial genome contains how many genes?
(a) 13
(b) 22
(c) 37
(d) 100
Q4. Which statement about the mitochondrial genetic code in humans is correct?
(a) UGA codes for tryptophan
(b) AUA codes for isoleucine
(c) AGA codes for arginine
(d) UAA codes for tyrosine
Q5. A mitochondrial disease is transmitted:
(a) From father to all sons
(b) From mother to all children
(c) From father to all daughters
(d) In a 3:1 Mendelian ratio
Q6. The condition in which a cell contains both normal and mutant mitochondrial DNA is called:
(a) Homoplasmy
(b) Heteroplasmy
(c) Heterozygosity
(d) Hemizygosity
Q7. Neutral petite mutants of yeast, when crossed with wild type, give:
(a) 2:2 segregation
(b) All petite progeny
(c) All normal progeny in all tetrads
(d) 1:1 petite and normal
Q8. Kappa particles in Paramecium aurelia are:
(a) Mitochondria
(b) Cytoplasmic symbiotic bacteria
(c) Plasmids of the nucleus
(d) Chloroplasts
Q9. The shell coiling in Limnaea is an example of:
(a) Organelle inheritance
(b) Maternal effect
(c) Genomic imprinting
(d) Sex-linked inheritance
Q10. Cytoplasmic male sterility in plants is controlled by genes in the:
(a) Nucleus only
(b) Mitochondria
(c) Ribosomes
(d) Golgi apparatus
Answer Key
Q1 | Q2 | Q3 | Q4 | Q5 | Q6 |
(b) | (b) | (c) | (a) | (b) | (b) |
Q7 | Q8 | Q9 | Q10 |
(c) | (b) | (b) | (b) |
11. Exam-Oriented Questions
A. One-Mark Questions (with answers)
1. What is extrachromosomal inheritance?
Ans: Inheritance of traits controlled by genes located outside the nucleus, in organelles, plasmids or cytoplasmic symbionts.
2. Name the scientists who first reported cytoplasmic inheritance in plants.
Ans: Carl Correns (Mirabilis jalapa) and Erwin Baur (Pelargonium zonale), 1909.
3. How many base pairs are in the human mitochondrial DNA?
Ans: 16,569 bp.
4. What is heteroplasmy?
Ans: Presence of more than one type (normal and mutant) of mtDNA in the same cell.
5. Expand LHON.
Ans: Leber hereditary optic neuropathy.
6. Who discovered petite mutants in yeast?
Ans: Boris Ephrussi (1949).
7. What are kappa particles?
Ans: Cytoplasmic symbiotic bacteria in killer Paramecium that produce the toxin paramecin.
8. Which Rf gene function is used in hybrid seed production?
Ans: Restoration of male fertility in CMS lines by nuclear restorer genes.
9. Name an organism showing maternal effect for shell coiling.
Ans: The snail Limnaea peregra.
10. What is an episome?
Ans: A plasmid that can exist autonomously or be integrated into the host chromosome (e.g. the F factor).
B. Two-Mark Questions (with answers)
1. List the criteria for identifying cytoplasmic inheritance.
Ans: Reciprocal crosses differ; progeny resemble the female parent; no Mendelian ratios; no linkage with nuclear genes; trait persists after nuclear substitution.
2. Why is mitochondrial inheritance maternal in humans?
Ans: The egg contributes almost all the cytoplasm and mitochondria of the zygote; sperm mitochondria are few and are ubiquitinated and destroyed after fertilisation.
3. What is the threshold effect in mitochondrial diseases?
Ans: Disease appears only when the proportion of mutant mtDNA in a tissue exceeds a critical level (often 60–90%), so energy-demanding tissues are affected first.
4. Distinguish between neutral and suppressive petites.
Ans: Neutral petites (large mtDNA deletions) give normal diploids and normal spores when crossed with wild type; suppressive petites give petite progeny in a high proportion of the cross.
5. What is cytoplasmic male sterility? State its use.
Ans: Failure of pollen production due to mitochondrial genes, restored by nuclear Rf genes; used for producing hybrid seed without emasculation.
6. Mention two effects of Wolbachia on its insect hosts.
Ans: Cytoplasmic incompatibility and male killing (also feminisation and parthenogenesis).
7. What is a maternal effect?
Ans: The phenotype of the offspring is determined by the nuclear genotype of the mother through gene products stored in the egg, giving delayed Mendelian inheritance.
8. Differentiate between plasmid and episome.
Ans: A plasmid is an extrachromosomal self-replicating DNA; an episome is a plasmid that can also integrate into the host chromosome, such as the F factor.
C. Five-Mark Questions (answer outlines)
1. Describe plastid inheritance in Mirabilis jalapa. Explain Correns' experiment.
Key points for answer:
– Branches: green, white and variegated; cross design with reciprocal crosses.
– Results: progeny resemble the seed (female) parent; variegated gives all three types.
– Table of crosses.
– Explanation: plastid mutation, cytoplasm from egg, random sorting of plastids.
– Contrast with Pelargonium (biparental), Chlamydomonas (uniparental) and gymnosperms (paternal).
2. Give an account of human mitochondrial DNA and the diseases caused by its mutations.
Key points for answer:
– Structure: 16,569 bp, 37 genes, D-loop, no introns, modified code.
– Maternal inheritance and the pedigree pattern.
– Heteroplasmy, bottleneck and threshold effect.
– Diseases: LHON, MERRF, MELAS, Kearns–Sayre, NARP.
– Applications: lineage tracing, forensic uses, mitochondrial replacement therapy.
3. Explain petite mutants of yeast and the poky mutant of Neurospora.
Key points for answer:
– Petite: respiratory deficient, small colonies (Ephrussi, 1949).
– Three types: segregational, neutral and suppressive, with crossing results.
– Poky: slow-growing strain, cytochrome defect (Mitchell and Mitchell, 1952).
– Maternal transmission through the protoperithecial parent.
– Conclusion: mitochondrial DNA carries these traits.
4. Write a note on infective heredity with reference to kappa particles in Paramecium.
Key points for answer:
– Killer and sensitive strains; paramecin and R bodies.
– Role of nuclear gene K and cytoplasmic kappa (Sonneborn, 1943).
– Effect of conjugation with and without cytoplasmic exchange.
– Other examples: sigma virus in Drosophila, Wolbachia, milk factor.
– Significance: cytoplasmic symbionts as hereditary elements.
5. Differentiate extrachromosomal inheritance from maternal effect with examples.
Key points for answer:
– Define each; genes involved (organelle vs nuclear).
– Limnaea coiling cross: F1, F2 and F3 results.
– Ephestia and Drosophila maternal-effect genes.
– Comparison table: segregation, persistence, examples.
– Conclusion about delayed Mendelian inheritance.
D. Additional Practice Questions
1. Explain cytoplasmic male sterility and its application in plant breeding.
2. Describe the chloroplast inheritance in Chlamydomonas.
3. Why do mitochondrial diseases show variable expression within the same family?
4. Explain the endosymbiotic theory with evidence.
5. Describe the types and functions of bacterial plasmids.
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