Organelles: nucleus, ER, Golgi, mitochondria, lysosomes, peroxisomes !
- Topic
Organelles are the cell's compartments; each has a job, and when one fails a specific disease appears.
Updated 2026-11-01
See it in 3D: Liver
What it is
The eukaryotic cell splits its work among membrane-bound compartments. The nucleus holds DNA, the endoplasmic reticulum and Golgi apparatus make and route proteins, mitochondria make ATP, and lysosomes and peroxisomes break down and detoxify. How much of each a cell has explains how it looks on H&E.
Function
- Secretory pathway: RER (synthesis) → cis Golgi → trans Golgi (sorting) → secretory vesicles or lysosomes.
- Degradation pathway: endosomes and autophagosomes fuse with lysosomes.
- A cell that secretes a lot of protein (plasma cell, pancreatic acinar cell) is basophilic; a steroid-making cell (adrenal cortex, Leydig cell) is eosinophilic and foamy.
Organelles: look, function and disease
| Organelle | How it looks | Function | Classic disease |
|---|---|---|---|
| Nucleus and nucleolus | Basophilic; dark heterochromatin, pale euchromatin; prominent nucleolus in active cells | Holds DNA, transcription, ribosome assembly | Large, irregular nuclei in dysplasia and cancer |
| Rough endoplasmic reticulum (RER) | Basophilic cytoplasm; Nissl bodies in neurons | Makes secreted and membrane proteins | Abundant in plasma cells (myeloma) |
| Smooth endoplasmic reticulum (SER) | Eosinophilic, foamy cytoplasm | Steroids, detoxification (cytochrome P450), calcium store (sarcoplasmic reticulum) | Expands in hepatocytes with enzyme-inducing drugs |
| Golgi apparatus | Pale zone beside the nucleus (perinuclear halo) | Glycosylates, sorts and packages; tags lysosomal enzymes with mannose-6-phosphate | I-cell disease |
| Mitochondrion | Eosinophilic, granular cytoplasm; double membrane with cristae on TEM | ATP by oxidative phosphorylation; starts intrinsic apoptosis; own DNA, inherited from the mother | Leigh syndrome, MELAS, ragged red fibres |
| Lysosome | Dense granules on TEM; not distinct on H&E | Acid hydrolases that digest the cell's own and foreign material | Tay-Sachs, Gaucher, Pompe |
| Peroxisome | Small bodies; very numerous in liver and kidney | Beta-oxidation of very-long-chain fatty acids, catalase, plasmalogens | Zellweger syndrome, adrenoleukodystrophy |
Clinical notes
- I-cell disease (mucolipidosis II): the Golgi phosphotransferase fails (GNPTAB gene), enzymes get no mannose-6-phosphate tag and leave the cell instead of reaching the lysosome; there are cytoplasmic inclusions and high lysosomal enzyme levels in plasma.
- Mitochondrial diseases hit brain and muscle hardest, the most energy-hungry tissues; when the defect is in mitochondrial DNA, it is inherited only from the mother.
- Lysosomal storage diseases: a missing hydrolase lets its substrate build up (GM2 ganglioside in Tay-Sachs, glucocerebroside in Gaucher).
Test yourself
Think of the answer, then tap the question to see it.
What defect causes I-cell disease?
Failure of the Golgi phosphotransferase (GNPTAB), so lysosomal enzymes are not tagged with mannose-6-phosphate and are secreted out of the cell.
Why does a plasma cell look basophilic on H&E?
It has abundant RER, whose ribosomal RNA takes up haematoxylin.
Which organelle oxidises very-long-chain fatty acids?
The peroxisome; its failure underlies Zellweger syndrome and adrenoleukodystrophy.
Why is a disease caused by a mitochondrial DNA variant inherited only from the mother?
The embryo's mitochondria come from the egg, not from the sperm.
See it in 3D
The structures of Durgical's 3D anatomy where it is found.
Related
- The cell membrane and transport
- Cytoskeleton: microfilaments, intermediate filaments, microtubules
- Cell injury, apoptosis and necrosis
- Electron microscopy: what it shows that light can't
- The neuron and synapse
Related conditions
- I-cell disease (mucolipidosis II)
- Leigh syndrome
- Tay–Sachs disease
- Gaucher disease
- Zellweger syndrome (Zellweger spectrum)
Educational content on normal microscopic structure and its clinical relevance; no substitute for studying slides or for a health professional's advice.
Sources: 3.2 The Cytoplasm and Cellular Organelles (OpenStax (Rice University), 2022); Mucolipidosis II alpha/beta (MedlinePlus Genetics (U.S. National Library of Medicine), 2024); Leigh syndrome (MedlinePlus Genetics (U.S. National Library of Medicine), 2024); Stains 02 (Digital Histology, 2024).
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Representative model, for educational purposes only.