Lesson-22.pdf). Content covers sections 22.1–22.12.Mango seeds grow mangoes; dogs produce puppies. The tendency of offspring to inherit parental characters is heredity. The science of heredity and of differences between parents and offspring is genetics. This NIOS Module 3 lesson covers Mendel’s pea experiments and laws; genetic terms; deviations (incomplete dominance, codominance, polygenes, lethals, pleiotropy); chromosomal theory; linkage and crossing over; sex determination (humans, birds, bees); X-linked inheritance; mitochondrial maternal inheritance; human karyotype and disorders; Rh factor; amniocentesis; and a brief idea of the human genome.
After this lesson you should explain heredity/genetics; describe Mendel’s work; define alleles, genotype, phenotype, etc.; explain non-Mendelian patterns; state chromosome theory; define linkage/crossing over; compare sex determination systems; describe major genetic disorders; and explain blood groups, Rh, amniocentesis and genomics. Notes follow textbook order only. Link to meiosis (recombination, segregation) and to L15 blood groups for transfusion logic.
Heredity is transmission of characters from one generation to the next (parents to offspring) via genes. Genetics studies the reasons for heredity and variation. Siblings differ except identical twins — such differences are variations (between parents and offspring, among siblings, or within a population).
Variation has survival value: if environment changes, some variants may adapt and save the population. Sources: mutation (sudden gene change); genetic recombination (gene exchange in meiosis; random mix of maternal and paternal chromosomes at fertilisation). Heritable variation generally arises from mutation and recombination.
Gregor Johann Mendel (1822–1884), Austrian monk, used garden pea (Pisum sativum), published 1865; rediscovered 1900 by Tschermak, Correns and De Vries. First to suggest clear principles of inheritance → father of genetics.
Method: pure tall × pure dwarf (anthers removed, stigma dusted with other pollen; reciprocal too). F₁ all tall. Self-pollinate F₁ → F₂ about 3 tall : 1 dwarf. He studied seven contrasting traits (flower colour, position, seed shape/colour, pod colour/shape, stem length). Monohybrid = one trait; dihybrid = two traits (e.g. tall red × dwarf white).
Why Mendel succeeded: short life cycle; self-pollinating bisexual flowers (true-breeding lines); complete dominance for all seven traits; genes either on different chromosomes or far apart (so independent assortment held — he did not discover linkage); careful pure-line crosses, bagging, counting, monohybrid then dihybrid, reciprocal and test crosses, statistics.
Experimental steps to memorise: (1) homozygous pure lines with contrasting characters; (2) remove stamens to prevent selfing; (3) dust stigma with desired pollen and bag flower; (4) collect and sow seeds by generation; (5) count phenotypes statistically; (6) one character at a time, then two; (7) reciprocal and test crosses to confirm. Seven traits: seed shape and colour, flower colour and position, pod colour and shape, stem length. All self-pollinating varieties bred true for one form generation after generation until deliberately crossed.
Genotype controls phenotype. Later work showed exceptions (incomplete dominance, codominance, polygenes, linkage).
Dihybrid gametes: F₁ TtRr produces TR, Tr, tR, tr in equal numbers if independent. Punnett square of 16 combinations yields 9 tall red, 3 tall white, 3 dwarf red, 1 dwarf white when T/R dominant. Segregation is universal because every meiosis separates homologues; independent assortment fails when genes are linked on one chromosome.
| Cross | F₂ phenotypic ratio |
|---|---|
| Monohybrid (complete dominance) | 3 : 1 |
| Dihybrid (independent assortment) | 9 : 3 : 3 : 1 |
| Incomplete dominance monohybrid | 1 : 2 : 1 |
| Test cross (heterozygote × recessive) | 1 : 1 |
Factor/gene — unit of inheritance; gene is a DNA segment. Alleles — alternative forms of a gene at the same locus (S/s smooth/wrinkled). Trait — visible character. Dominant expresses in heterozygote; recessive only when homozygous. Genotype — genetic constitution (SS, Ss, ss); phenotype — outward appearance. Homozygous identical alleles (SS); heterozygous dissimilar (Ss). P, F₁, F₂ generations. Monohybrid/dihybrid crosses. Hybridisation — crossing different types for desirable traits. Test cross — F₁ × homozygous recessive → 1:1 if F₁ heterozygous. Reciprocal cross — reverse sexes of parents.
Incomplete dominance (four o’clock Mirabilis, snapdragon): RR red × rr white → F₁ all pink Rr; F₂ 1 red : 2 pink : 1 white (phenotype = genotype ratio 1:2:1). Heterozygote intermediate.
Multiple alleles and codominance — ABO blood groups: IA, IB codominant; i (or io) recessive. Genotypes: IAIA or IAi → A; IBIB or IBi → B; IAIB → AB; ii → O. Parents AB × O → all children A or B (IAi or IBi), none O or AB only from those parents alone.
Lethal genes: yellow mouse allele Y; homozygous YY dies as zygote; only heterozygotes yellow. Recessive lethals kill only when homozygous.
Pleiotropy: one gene affects several phenotypes (white-eye gene in Drosophila also affects wings/abdomen).
Polygenic (quantitative) inheritance: many genes additive — human height and skin colour, wheat kernel colour; continuous variation; each gene contributes a little pigment/height. Three to four genes may contribute to human skin pigment — hence continuous range from very fair to very dark. “Why so many complexions?” is answered by polygenes, not single Mendelian pairs.
Codominance vs incomplete dominance: in codominance both alleles fully show (AB blood antigens both present); in incomplete dominance the heterozygote is intermediate (pink). Multiple alleles: more than two forms of a gene in the population (ABO has three), though an individual still carries only two.
Sutton and Boveri (1902): chromosomes from two parents meet in zygote and separate in meiosis — same behaviour as Mendelian factors. Genes are on chromosomes (DNA segments). Homologous pairs; gametes haploid (n); zygote diploid (2n). Humans 23 pairs.
Linkage: Bateson & Punnett dihybrid in sweet pea gave ~7:1:1:7 not 9:3:3:1 — genes on same chromosome inherited together = linked. Linkage group = genes on one chromosome that tend to travel together.
Crossing over: physical exchange between non-sister chromatids of homologues at chiasmata in prophase I of meiosis — separates linked genes; produces recombinant gametes. Heterozygotes can form four gamete types: parental + recombinant.
Chromosome theory points: (1) body cells diploid with maternal and paternal homologues; (2) homologues separate at meiosis into gametes; (3) genes lie linearly on chromosomes. Molecular update: chromosome = DNA + proteins; genes = DNA segments. Sweet pea linkage (Bateson and Punnett) is the classic counterexample to free assortment when genes sit on one chromosome. Recombination frequency rises with distance between loci — closer genes stay linked more often.
Humans XX–XY: female XX homogametic (all eggs X); male XY heterogametic (X or Y sperm). Egg + X sperm → girl; egg + Y sperm → boy. Chance decides sex; Y needed for maleness. No parent is “to blame.” Autosomes are the 22 pairs that are not sex chromosomes. Sex chromosomes are XX or XY; presence of Y produces male features in the textbook account.
Birds ZW–ZZ: male ZZ homogametic; female ZW heterogametic — female produces two egg types; opposite of mammals.
Honey bees (haplodiploidy): fertilised eggs → diploid females (workers/queen); unfertilised eggs → haploid males (drones). “Males have no father and cannot have sons but have a grandfather” — male from unfertilised egg of diploid mother; his daughters get his genes then produce grandsons. Only females from sexual fertilisation.
Genes on X are sex-linked. Affected male (XhY) passes defective X only to daughters. Carrier female (XHXh) passes it to half sons and half daughters. Sons express recessive X-linked traits (one X, no partner allele on Y). Daughters need two defective copies to be affected; heterozygotes are carriers. Path: father → daughter → grandson = criss-cross inheritance.
Examples: red–green colour blindness; haemophilia (blood fails to clot). Colour-blind man × normal woman whose parents had normal vision → sons not colour-blind if mother not carrier (sons get mother’s X). Carrier woman × normal man → 50% sons colour-blind/haemophilic, 50% daughters carriers among those inheriting the bad X. Affected males more common because one recessive allele on the single X is enough.
Why called criss-cross: trait appears to zigzag sexes across generations — grandfather to grandson via carrier daughter. Father never passes his X to sons (sons get Y from father), so no male-to-male X-linked transmission.
Mitochondrial inheritance is maternal: mitochondria (and their DNA) come with the egg; sperm contributes little cytoplasm. Some disorders track mother’s family line.
Human karyotype: 2n = 46; 22 pairs autosomes + XX or XY; arranged in 7 groups A–G by size and centromere; sex chromosomes last. Presence of Y → male phenotype; absence of Y → female (with defects if XO).
Down’s (mongolism): 47 chromosomes, trisomy 21 — mental retardation, thick tongue, characteristic face; risk rises with maternal age >40.
Klinefelter’s: 47, XXY male — tall, sterile, gynaecomastia, often retarded.
Turner’s: 45, XO female — short, webbed neck, incomplete breasts, retarded.
Thalassemia: autosomal recessive defective Hb; frequent transfusions; homozygous sick; parents may be carriers.
Sickle-cell anaemia: autosomal mutation; homozygous often fatal; heterozygotes half-normal RBCs and malaria resistance (parasite thrives poorly in sickle cells).
Rh factor: antigen on RBC. Rh⁻ mother + Rh⁺ foetus → mother makes antibodies; first pregnancy often mild; later Rh⁺ foetuses risk haemolytic disease (erythroblastosis foetalis). Modern treatment after delivery destroys Rh antigens in mother.
Amniocentesis: sample amniotic fluid → culture foetal cells → analyse chromosomes for genetic defects; if incurable, pregnancy may be terminated. Illegal to use only for sex determination of the unborn.
Human genome: all genes on the haploid set (n). Genomics = study of genomes. Mapped largely by ~2003; ~20,000–25,000 genes; ~3 billion base pairs; only ~1.5% protein-coding; rest regulation, non-coding, promoters (e.g. TATA), rRNA/tRNA genes. Hope for gene therapy of disorders.
Heredity vs genetics vs variation; Mendel’s methods and three laws; 3:1 and 9:3:3:1; terms list; incomplete dominance 1:2:1; ABO genotypes; lethal/pleiotropy/polygenic; Sutton–Boveri; linkage vs crossing over; human/bird/bee sex determination; criss-cross X-linked; mitochondrial maternal; Down/Klinefelter/Turner; colour blindness/haemophilia; thalassemia/sickle; Rh; amniocentesis; genome numbers.
Universal law: segregation. Complexions: polygenic skin colour. Colour-blind man × carrier woman: work Punnett for sons/daughters. Honey-bee males: unfertilised eggs.
Use Formula Sheet; drill 10 MCQs and 20 flashcards. Prioritise laws, ratios, ABO, sex systems, and syndrome chromosome numbers.
Mendel’s seven traits: seed shape (round/wrinkled), seed colour (yellow/green), flower colour (purple/white), flower position (axial/terminal), pod colour (green/yellow), pod shape (inflated/constricted), stem length (tall/dwarf). All showed complete dominance, which made 3:1 and 9:3:3:1 clean. Independent assortment worked because his gene pairs were not tightly linked — luck of trait choice.
Worked monohybrid dominance: TT × tt → F₁ Tt all tall → F₂ genotypes 1 TT : 2 Tt : 1 tt → phenotypes 3 tall : 1 dwarf. Incomplete: RR × rr → Rr pink → F₂ 1:2:1 both genotype and phenotype. Dihybrid independent: TTRR × ttrr → F₁ TtRr → F₂ 9 tall red : 3 tall white : 3 dwarf red : 1 dwarf white. Test cross Tt × tt → 1 tall : 1 dwarf confirms heterozygosity.
ABO parents AB × O: gametes IA or IB from first; i from second → children IAi (A) or IBi (B) only. Codominance means both IA and IB fully express in AB blood.
Linkage breaks independent assortment; crossing over restores some recombinants — frequency reflects distance between genes. Chromosome theory unifies Mendel with cytology: factors are genes on chromosomes.
Sex determination chance: half X and half Y sperm on average — population sex ratio near 1:1. Birds reverse which sex is heterogametic. Bees separate sex from fertilisation itself (haploid males).
X-linked pedigree rule: affected males more common; no father-to-son X transmission of the trait gene (sons get Y from father); carrier mothers → half sons affected. Haemophilia historically in royal pedigrees as textbook illustration of X-linkage.
Rh: problem is mother Rh⁻, foetus Rh⁺ (from father); maternal antibodies attack foetal RBCs in later pregnancies. Treatment after first delivery protects later pregnancies.
Closed-book drill: (1) define heredity, genetics, variation; (2) three Mendel laws + which universal; (3) monohybrid & dihybrid ratios; (4) ten genetic terms; (5) incomplete dominance example & ratio; (6) ABO table; (7) lethal, pleiotropy, polygenic one line each; (8) chromosome theory; (9) linkage & crossing over; (10) human/bird/bee sex; (11) criss-cross definition + two diseases; (12) mitochondrial maternal; (13) three aneuploid syndromes; (14) Rh problem; (15) amniocentesis steps & ban on sex selection; (16) genome definition. Completing these covers Lesson 22 terminals.
Tall TT × dwarf tt → F₁ all Tt tall. Self → F₂ phenotypes 3 tall : 1 dwarf; genotypes 1 TT : 2 Tt : 1 tt. If incomplete, same genotypes give 1:2:1 phenotypes. Dihybrid F₁ TtRr selfed → 9:3:3:1 when unlinked. Test cross TtRr × ttrr → 1:1:1:1 of four phenotypes if independent; excess parental types if linked.
ABO: IAIB × ii → children IAi (group A) or IBi (group B). IAi × IBi can give A, B, AB, or O. Rh: antigen on RBC; Rh⁻ mother + Rh⁺ foetus → maternal antibodies; risk rises in later pregnancies; modern post-delivery treatment reduces risk.
Honey bee statement: male from unfertilised egg has mother but no father; he produces sperm mitotically and cannot father sons who are haploid from unfertilised eggs of daughters — but his daughter’s sons are his grandsons. Females diploid from fertilised eggs.
Syndrome quick list: Down 47 (+21) mental retardation, thick tongue, face; risk older mothers. Klinefelter 47 XXY sterile male with breasts. Turner 45 XO webbed neck, incomplete breasts. Thalassemia autosomal recessive Hb defect, transfusions. Sickle cell homozygous severe; heterozygote malaria advantage.
Amniocentesis steps: syringe amniotic fluid → foetal skin cells → culture → chromosome analysis → counsel if serious defect. Illegal solely for foetal sex. Genome: haploid gene set; genomics is the study; ~20–25 thousand genes; ~3 billion base pairs; ~1.5% coding.
Quick formula strip: heredity/genetics/variation; segregation universal; 3:1; 9:3:3:1; 1:2:1 incomplete; ABO IAIBi; linkage vs crossover; XX/XY · ZW/ZZ · n/2n bees; X-linked criss-cross; mtDNA mother; 47+21 · XXY · XO; Rh; amniocentesis; genome. Say each with one example. You are exam-ready when ratios, ABO, sex systems, and syndrome numbers come without notes.
Rediscovery note: Mendel’s paper of 1865 was ignored until 1900 when Hugo de Vries, Correns and Tschermak independently found the same laws — then Mendel was recognised as first. Factors became genes; alleles are alternative forms. Homozygous pure tall is TT; heterozygous tall is Tt; only tt is dwarf. Phenotype “tall” hides two genotypes. That distinction is the heart of every Mendel problem on the paper. Variation survival value: if climate or disease changes, some genotypes in a mixed population may live when pure clones would die. Genetics therefore sits at the centre of both medicine (disorders, blood groups, Rh) and evolution (variation raw material). Colour-blind man marries carrier woman: sons may be normal or colour-blind; daughters may be normal, carriers, or colour-blind depending on X combinations — always draw the Punnett with X and Y carefully. Human female is homogametic because she produces only X eggs; male is heterogametic because he produces X and Y sperms. Bird female is the heterogametic sex instead. Keep those three systems distinct for matching questions on the NIOS board examination paper for this academic year of senior secondary biology study workbook notes.
Most exam-important points from this chapter:
Segregation always; dominance often; independent assortment if unlinked. Monohybrid 3:1; dihybrid 9:3:3:1; test cross 1:1. Pea, pure lines, careful counts.
Allele, genotype, phenotype, homo/hetero. Incomplete → intermediate 1:2:1. ABO codominance + multiple alleles. Lethal, pleiotropy, polygenes break simple ratios.
Sutton–Boveri: genes on chromosomes. Linkage groups; crossing over in prophase I makes recombinants. DNA segments = genes.
Human XX/XY; bird ZW/ZZ; bee haplodiploidy. X-linked colour blindness/haemophilia: males express; females carry; criss-cross pattern.
Down 47(+21), Klinefelter XXY, Turner XO. Rh⁻ mother risk. Amniocentesis for foetal chromosomes not sex selection. Genome = haploid gene set.
PE-only questions for this chapter only. 6 item(s). No overlap with other lessons. Tap Show answer after you try each question.
Q1. A cross between the F1 progeny and the homozygous recessive parent is known as
Why it clicks: F1 × homozygous recessive = test cross to reveal genotype.
Q2. The phenotypic ratio, in case of incomplete dominance in Mirabilis jalapa, is
Why it clicks: Incomplete dominance (Mirabilis): red : pink : white = 1 : 2 : 1.
Q3. A cross was made between a tall pea plant with red flowers (TTRR) and a dwarf pea plant with white flowers (ttrr). Work out the cross up to F2 generation. Write the phenotypic ratio of F2 generation. 3 b o
Why it clicks: Classic Mendel dihybrid 9:3:3:1.
Q4. Read the following passage and fill in the blanks with appropriat e words. 2 (Attempt any two parts A-D) Criss Cross inheritance in humans A.and B.are examples of sex-linked inheritance in humans. The defective gene is located on C. chromosome. Thus a single defective gene causes disease in males while two defective genes (D. condition) only can cause the disease in females. 12 ]
Why it clicks: X-linked: males express with one copy; females need two.
Q5. (b) A tall pea plant with red flowers (TTRR) is crossed with white dwarf plants (ttrr). Work out the phenotypic ratio in F2 for this cross. (b) U U c (TTRR) c (ttrr) U
Why it clicks: TTRR × ttrr → F1 TtRr → F2 9:3:3:1.
Q6. (II) Haemophilia is a sex linked disease in human beings. A carrier female has married a normal male. Show the genotype of both the individuals. What will be the phenotype of their progeny both daughter and son, with regard to the disease?
Why it clicks: Criss-cross: sons get mothers X.
Six problems spanning this chapter’s NIOS Biology (314) syllabus. Every question is built from the notes and formula sheet: solve with definitions and equations first, then read the formal textbook-style write-up, the easy explanation, and the topic in depth (key relations, meaning, exam tips). If the question says draw, a labelled pencil sketch is provided. Explanations open by default.
In a monohybrid cross Tt × Tt (complete dominance), what are phenotypic and genotypic ratios in F₂? Draw a Punnett square.
Final answer: 3:1 phenotype; 1:2:1 genotype
Mendel’s segregation explains monohybrid ratios.
Key relations: F₂ phenotype 3:1; Genotype 1:2:1 for monohybrid. State the definition or law first (NIOS style), use correct biological terms, and end with a clear boxed conclusion.
Three look dominant, one recessive; genes split 1:2:1.
Read the question once for the idea, once for the details. Write the definition or equation, then apply it. Check labels and units if any numbers appear.
Always state assumptions: complete dominance and no lethality.
Linked to chapter notes (L22). Remember: F₂ phenotype 3:1; Genotype 1:2:1 for monohybrid. Most exam errors mix up similar terms, reverse cause and effect, or skip labelled diagrams.
Open with a one-line definition, then use: F₂ phenotype 3:1; Genotype 1:2:1 for monohybrid. For diagram questions, label every part asked and keep lines neat.
Define allele, homozygous, and phenotype.
Final answer: Allele=gene form; homozygous=same pair; phenotype=seen trait
Precise genetic vocabulary is essential for NIOS answers.
Key relations: Allele: alternate forms of gene; Homozygous: identical alleles; Phenotype: appearance. State the definition or law first (NIOS style), use correct biological terms, and end with a clear boxed conclusion.
Alleles are versions; homozygous means matching pair; phenotype is what you see.
Read the question once for the idea, once for the details. Write the definition or equation, then apply it. Check labels and units if any numbers appear.
Genotype is the genetic formula (Tt).
Linked to chapter notes (L22). Remember: Allele: alternate forms of gene; Homozygous: identical alleles; Phenotype: appearance. Most exam errors mix up similar terms, reverse cause and effect, or skip labelled diagrams.
Open with a one-line definition, then use: Allele: alternate forms of gene; Homozygous: identical alleles; Phenotype: appearance. For diagram questions, label every part asked and keep lines neat.
What phenotypic ratio does a dihybrid cross (independent assortment, complete dominance) give in F₂?
Final answer: 9:3:3:1
Mendel’s second law: genes on different chromosomes assort independently.
Key relations: F₂ dihybrid 9:3:3:1. State the definition or law first (NIOS style), use correct biological terms, and end with a clear boxed conclusion.
Two traits free to mix give the classic 9:3:3:1 split.
Read the question once for the idea, once for the details. Write the definition or equation, then apply it. Check labels and units if any numbers appear.
Linkage modifies this ratio—advanced caveat.
Linked to chapter notes (L22). Remember: F₂ dihybrid 9:3:3:1. Most exam errors mix up similar terms, reverse cause and effect, or skip labelled diagrams.
Open with a one-line definition, then use: F₂ dihybrid 9:3:3:1. For diagram questions, label every part asked and keep lines neat.
How does a test cross reveal whether a tall plant (T_) is TT or Tt?
Final answer: Cross with tt; ratios distinguish TT vs Tt
Test cross is a diagnostic tool for genotype of dominant phenotype.
Key relations: Unknown dominant × recessive homozygous; 1:1 if heterozygous. State the definition or law first (NIOS style), use correct biological terms, and end with a clear boxed conclusion.
Breed mystery tall with short; if any short kids, mystery was hybrid.
Read the question once for the idea, once for the details. Write the definition or equation, then apply it. Check labels and units if any numbers appear.
Used by Mendel conceptually for purity tests.
Linked to chapter notes (L22). Remember: Unknown dominant × recessive homozygous; 1:1 if heterozygous. Most exam errors mix up similar terms, reverse cause and effect, or skip labelled diagrams.
Open with a one-line definition, then use: Unknown dominant × recessive homozygous; 1:1 if heterozygous. For diagram questions, label every part asked and keep lines neat.
Why do fathers determine the sex of the child in humans (XY system)?
Final answer: Sperm X or Y decides sex
Human sex chromosomes follow XX/XY mechanism.
Key relations: XX female; XY male; Father determines sex of child. State the definition or law first (NIOS style), use correct biological terms, and end with a clear boxed conclusion.
Mom always gives X; dad’s X or Y chooses girl or boy.
Read the question once for the idea, once for the details. Write the definition or equation, then apply it. Check labels and units if any numbers appear.
Not related to lunar myths—purely chromosomal.
Linked to chapter notes (L22). Remember: XX female; XY male; Father determines sex of child. Most exam errors mix up similar terms, reverse cause and effect, or skip labelled diagrams.
Open with a one-line definition, then use: XX female; XY male; Father determines sex of child. For diagram questions, label every part asked and keep lines neat.
Define mutation and state one importance in evolution/breeding.
Final answer: Heritable DNA change; creates new variation
Mutations may be harmful, neutral or rarely beneficial.
Key relations: Mutation: sudden heritable change in DNA/gene/chromosome. State the definition or law first (NIOS style), use correct biological terms, and end with a clear boxed conclusion.
A mutation is a genetic typo that can stick in kids—fuel for evolution.
Read the question once for the idea, once for the details. Write the definition or equation, then apply it. Check labels and units if any numbers appear.
Not all mutations are in body cells—germline matters for inheritance.
Linked to chapter notes (L22). Remember: Mutation: sudden heritable change in DNA/gene/chromosome. Most exam errors mix up similar terms, reverse cause and effect, or skip labelled diagrams.
Open with a one-line definition, then use: Mutation: sudden heritable change in DNA/gene/chromosome. For diagram questions, label every part asked and keep lines neat.