Mechanisms of Development
High-Yield Summary
- Cell fate path: specification (reversible) → determination (irreversible, morphogen-guided) → differentiation (builds actual structures/machinery).
- Stem cell potency, most to least flexible: totipotent (any cell + placenta) → pluripotent (any germ layer, no placenta) → multipotent (one lineage, e.g. hematopoietic stem cells).
- 4 signaling types by range/contact: autocrine (self), juxtacrine (direct contact/gap junctions), paracrine (short diffusion), endocrine (bloodstream, long range).
- Morphogen gradients: concentration determines gene expression/fate — cells near the source get one fate, far cells get another.
- Apoptosis = programmed, controlled, non-inflammatory (phagocytosed as apoptotic bodies). Necrosis = uncontrolled, injury-driven, inflammatory.
- Cellular senescence: telomeres shorten each division → Hayflick limit reached → cell stops dividing (still alive, non-dividing) — a driver of aging.
Key Terms
- Morphogen
- Chemical signal guiding determination; forms a concentration gradient that assigns different fates to cells at different distances from the source.
- Competency
- A cell's ability to respond to a given inducing/morphogen signal.
- Reciprocal induction
- Two tissues alternately signal each other, each refining the other's fate/structure.
- Apoptotic bodies
- Small membrane-bound fragments produced when an apoptotic cell breaks apart, cleared via phagocytosis without inflammation.
- Hayflick limit
- The replicative limit reached once telomeres shorten past a critical point, triggering cellular senescence.
Stem Cell Potency
| Type | Range of Fates |
|---|---|
| Totipotent | Any cell type + extra-embryonic tissue (placenta) — fertilized egg, early embryo cells |
| Pluripotent | Any cell from ectoderm/mesoderm/endoderm — no placental tissue |
| Multipotent | Restricted subset within one lineage — e.g. hematopoietic stem cells → blood cell types only |
Apoptosis vs. Necrosis
| Apoptosis | Necrosis |
|---|---|
| Programmed, controlled | Uncontrolled, from injury/trauma |
| Cell shrinks, DNA condenses, breaks into apoptotic bodies | Cell swells, contents leak, organelles break down |
| No inflammation (cleared by phagocytosis) | Triggers inflammation, damages surrounding tissue |
Cell Signaling Types
| Type | Range / Mechanism |
|---|---|
| Autocrine | Cell signals itself |
| Juxtacrine | Direct contact (e.g. gap junctions) |
| Paracrine | Short-range diffusion to nearby neighbor |
| Endocrine | Long-range via bloodstream (hormone) |
Common MCAT Trap
- Specification is reversible; determination is NOT — a common source of confused wording on passages.
- Pluripotent cells cannot form placental tissue (only totipotent can) — a frequently tested distinction.
- Stronger morphogen signal ≠ "more differentiated" cell — concentration determines WHICH fate/gene set activates, not degree of differentiation.
Quick Recall
What distinguishes totipotent from pluripotent stem cells?
Which type of cell death is non-inflammatory and programmed?
What triggers cellular senescence?
What signaling type acts through direct cell-to-cell contact, e.g. gap junctions?