The document discusses glycosylation and adp-ribosylation, two key post-translational modifications that proteins undergo, influenced by bacterial toxins. These modifications can disrupt cellular processes, leading to cell death and various diseases, with specific examples including cholera, diphtheria, and botulinum toxins. Additionally, the document outlines seven distinct secretion mechanisms used by bacteria to release toxins, which are vital for understanding and potentially treating related diseases.

1. Glycosylation is the process of adding sugar molecules to proteins. It is a common post-translational
modification that occurs in all cells. Glycosylation can affect the structure, function, and localization
of proteins.
Toxins can also modify proteins by glycosylation. This is called toxin-induced glycosylation. Toxin-
induced glycosylation can have a variety of effects on cells, including:
• Inactivating proteins by blocking their function
• Changing the localization of proteins
• Regulating the activity of proteins
• Signalling to other proteins
Toxin-induced glycosylation is a mechanism by which toxins can disrupt cellular processes and cause
disease. Some examples of toxins that induce glycosylation include:
• Clostridium difficile toxins A and B: These toxins glycosylate small GTPases, which
are proteins involved in cell signalling. Glycosylation of these proteins inhibits their function, which
can lead to cell death
• Cholera toxin: This toxin ADP-ribosylates the Gαs subunit of a G protein, which leads
to the activation of adenylate cyclase and the production of cyclic AMP. This increase in cyclic AMP
causes cells to secrete water and electrolytes, which can lead to diarrhoea.
• Shiga toxin: This toxin glycosylate the ribosome, which is the organelle that makes
proteins. Glycosylation of the ribosome inhibits protein synthesis, which can lead to cell death.
Toxin-induced glycosylation is a complex and versatile mechanism that can be used by toxins to
disrupt a variety of cellular processes. It is an important area of research for understanding the
mechanisms of disease and developing new treatments.
ADP-ribosylation is a post-translational modification that is catalyzed by enzymes called ADP-
ribosyltransferases (ARTs). ADP-ribosyltransferases can be found in both bacteria and eukaryotes.
Toxins produced by some bacteria can also ADP-ribosylate proteins in host cells. This can have a
variety of effects on the cell, depending on the protein that is ADP-ribosylated and the type of toxin.
Some examples of bacterial toxins that ADP-ribosylate proteins include:
• Cholera toxin: This toxin ADP-ribosylates the Gαs subunit of a G protein, which leads
to the activation of adenylate cyclase and the production of cyclic AMP. This increase in cyclic AMP
causes cells to secrete water and electrolytes, which can lead to diarrhea.
• Diphtheria toxin: This toxin ADP-ribosylates elongation factor 2, which is an enzyme
that is essential for protein synthesis. ADP-ribosylation of elongation factor 2 blocks protein
synthesis, which can lead to cell death.

2. • Botulinum toxin: This toxin ADP-ribosylates SNAP-25, a protein that is involved in
the release of neurotransmitters. ADP-ribosylation of SNAP-25 blocks neurotransmitter release,
which can lead to paralysis.
• Pertussis toxin: This toxin ADP-ribosylates Gi, a G protein that is involved in signal
transduction. ADP-ribosylation of Gi inhibits signal transduction, which can lead to a variety of
symptoms, including cough, fever, and respiratory distress.
There are seven different secretion mechanisms of bacterial toxins, classified as Type I to Type VII.
These mechanisms are used by bacteria to secrete toxins, enzymes, and other proteins out of the cell.
Type I secretion system (T1SS) is the most common secretion system in Gram-negative bacteria. It
is used to secrete a variety of toxins, including cholera toxin, diphtheria toxin, and pertussis toxin.
The T1SS is a complex system that consists of several proteins, including a pore-forming protein, an
usher protein, and a translocation protein.
Type II secretion system (T2SS) is also common in Gram-negative bacteria. It is used to secrete a
variety of toxins, including Shiga toxin, ETEC enterotoxin, and Y. pestis pesticin. The T2SS is similar
to the T1SS, but it is more complex and can secrete larger proteins.
Type III secretion system (T3SS) is used by a variety of Gram-negative bacteria, including
Salmonella, Shigella, and Yersinia. It is a complex system that is used to inject proteins directly into
host cells. The T3SS is responsible for the symptoms of diseases such as typhoid fever, dysentery,
and plague.
Type IV secretion system (T4SS) is used by a variety of Gram-positive bacteria, including Listeria,
Clostridium, and Staphylococcus. It is used to inject proteins directly into host cells. The T4SS is
responsible for the symptoms of diseases such as listeriosis, botulism, and toxic shock syndrome.
Type V secretion system (T5SS) is used by a small number of bacteria, including Pseudomonas
aeruginosa and Vibrio cholerae. It is used to secrete proteins that can degrade host tissues. The T5SS
is responsible for the symptoms of diseases such as P. aeruginosa pneumonia and V. cholerae
diarrhea.
Type VI secretion system (T6SS) is used by a small number of bacteria, including Mycobacterium
tuberculosis and Salmonella typhimurium. It is used to secrete proteins that can disrupt host cell

3. signaling. The T6SS is responsible for the symptoms of diseases such as tuberculosis and
salmonellosis.
Type VII secretion system (T7SS) is the least common secretion system. It is used by a small number
of bacteria, including Campylobacter jejuni and Helicobacter pylori. It is used to secrete proteins that
can disrupt host cell metabolism. The T7SS is responsible for the symptoms of diseases such as
Campylobacteriosis and Helicobacter pylori gastritis.
The different secretion mechanisms of bacterial toxins are used by bacteria to cause a variety of
diseases. By understanding these mechanisms, scientists can develop new ways to prevent and treat
these diseases.