Evolution

Darwin, Wallace, and the synthesis

Charles Darwin's 1859 On the Origin of Species and Alfred Russel Wallace's independent 1858 manuscript jointly established natural selection: heritable variation, overproduction of offspring, struggle for existence, and differential reproductive success. Punjab Textbook Board Biology XII Chapter 21 and Campbell 12e Chapters 22–25 layer this with twentieth-century population genetics from R. A. Fisher, J. B. S. Haldane, and Sewall Wright (the Modern Synthesis, 1930s–40s) and twenty-first-century molecular evolution. Lamarck's 1809 inheritance of acquired characteristics is now mostly historical, though epigenetic inheritance has revived limited interest.

Lines of evidence

Fossils document descent with modification: Tiktaalik roseae (375 Mya, Devonian) bridges fish and tetrapods with wrist bones in fin-like limbs; Archaeopteryx (150 Mya) shows reptilian teeth and tail with feathers and wings; whale ancestors (Pakicetus, Ambulocetus, Basilosaurus) show progressive aquatic adaptation. Comparative anatomy reveals homologous structures (vertebrate forelimbs share humerus-radius-ulna-carpals despite different functions), analogous structures (bat wing vs insect wing — same function, different origin), and vestigial structures (whale pelvis, human appendix and coccyx). Embryology: pharyngeal arches in all vertebrate embryos point to common ancestry. Biogeography: marsupial radiation in Australia and finch radiation in the Galápagos. Molecular evidence: cytochrome c sequences differ from human by 0 amino acids in chimpanzee, 1 in rhesus monkey, ~13 in chicken, and ~44 in yeast.

Mechanisms of evolutionary change

Five forces alter allele frequencies. Mutation (rate ≈ 10⁻⁸ per bp per generation in humans) is the ultimate source of variation. Natural selection acts on heritable phenotypic variation; modes include directional (peppered moth shifting from light to dark in industrial Britain — Kettlewell, 1955), stabilising (human birth weight optimum ~3.5 kg), and disruptive (African seedcrackers with bimodal beak sizes). Genetic drift dominates in small populations — bottleneck (cheetahs, founder effects in Amish populations). Gene flow homogenises populations through migration. Non-random mating (assortative mating, sexual selection — peacock tails as Zahavi's handicap principle, 1975) reshapes genotype frequencies without altering allele frequencies.

Hardy-Weinberg and population genetics

The Hardy-Weinberg theorem (1908) predicts that under no mutation, no migration, no selection, no drift, and random mating, allele frequencies stay constant: p² + 2pq + q² = 1. Deviations diagnose evolution. For a recessive disease with q² = 1/10 000 (cystic fibrosis-like), q = 0.01 and 2pq ≈ 0.02, so 1 in 50 are carriers. Selection against homozygote AA with fitness w_AA, etc., changes Δq predictably; sickle-cell HbS is maintained at frequencies up to 0.15 in malaria-endemic regions because heterozygotes (HbAS) have ~10× lower mortality from Plasmodium falciparum — a textbook case of balanced polymorphism.

Speciation and phylogenetics

Ernst Mayr's biological species concept (1942): species are groups of actually or potentially interbreeding populations reproductively isolated from other such groups. Allopatric speciation requires geographic isolation (Galápagos finches, ~14 species from a common South American ancestor). Sympatric speciation occurs without geographic separation, often through polyploidy (frequent in plants — wheat Triticum aestivum is hexaploid AABBDD). Reproductive isolation arises pre-zygotically (habitat, temporal, behavioural, mechanical, gametic) or post-zygotically (hybrid inviability, sterility — mules, hybrid breakdown). Cladistics builds phylogenies from shared derived characters (synapomorphies); molecular clocks calibrate divergence times. The human–chimpanzee split is dated to ~6–7 Mya from molecular and fossil evidence, with Sahelanthropus tchadensis as an early candidate hominin.