A cellular junction is made up of cytoskeletal filaments and cell adhesion molecules, which connect cytoskeletal elements between adjacent cells. There are three types of cytoskeletal filaments: microfilaments (actin filaments), intermediate filaments, and microtubules. A cellular junction usually utilizes connections with either actin filaments or intermediate filaments. Desmosomes and hemidesmosomes use intermediate filaments (particularly keratin) whereas tight junctions, adherens junctions, and focal adhesion junctions use actin filaments.

The question states that the autoimmune disease attacks occludin proteins. Recall that the occludin proteins are cell adhesion molecules found in tight junctions. Tight junctions, as the name implies, form sealing junctions that restrict the passage of molecules between adjacent cells. A lack of occludin proteins will decrease the amount of tight junctions and, subsequently, will increase the exchange of molecules between cells.

Cadherin proteins are also cell adhesion molecules, but they are found in adherens junctions. They do not depend on occludin proteins and, therefore, will not be affected by this disease. Tight junctions do require actin filaments and will be affected by this autoimmune disease; however, other actin utilizing junctions, such as adherens junctions and focal adhesions, don’t use occludin proteins and will not be affected.

Cell junctions are connections between a cell and its environment. There are two types of junctions: cell-cell and cell-matrix. Cell-cell junctions occur between adjacent cells and include tight junctions (or Zona Occludens), desmosomes, and adherens junctions. Cell-matrix junctions form between a cell and the extracellular matrix, and include hemidesmosomes and focal adhesions. 

Both desmosomes and hemidesmosmes use keratin, a type of intermediate filament; therefore, both use the same cytoskeletal filament. Tight junctions, focal adhesions, and adherens junctions utilize actin filaments, the other cytoskeletal filament found in cell junctions.

Desmosomes are spot-like junctions that occur between cells (cell-cell junction). Hemidesmosomes, or “half” desmosomes, are also spot-like junctions, but they occur between a cell and the extracellular matrix. Cell adhesion molecules (CAMs) are found in all cell junctions. They are typically found bound to the cytoskeletal filament, and function to hold the junction together. The CAM for desmosomes is a cadherin-like protein called desmoglein, whereas the CAM for hemidesmosomes is integrin. Epithelial cells typically have all types of cell junctions between adjacent cells, not just desmosomes. 

Cell walls are present in virtually all prokaryotic cells, but are also found in certain eukayotic domains (such as plants and fungi). As such, the presence of a cell wall cannot be used to distinguish between prokaryotic and eukaryotic cells.

Chyme from the stomach is transferred to the small intestine through the pyloric sphincter. The highly-acidic chyme is then neutralized in the duodenum of the small intestine. The majority of the small intestine has a pH between 6 and 7.

Peroxisomes are involved in the metabolism of hydrogen peroxide and very long chain fatty acids. They are also known to produce plasmalogen, an important phospholipid found in myelin, without which disorders of the nervous system can arise. Lysosomes, not peroxisomes, store acid hydrolases such as lipase.

Lysosomes are the cell's repository of digestive enzymes. When these merge with phagosomes, the result is a vesicle that is able to digest phagocytosed material.

Spectrin and ankyrin are structural proteins associated with the cytoskeleton, especially in muscle cells.

The lysosome is the main storage site for digestive proteins. These digestive proteins are then released into the phagosome to form the phagolysosome. This phagolysosome is then able to digest phagocytosed material and render it harmless to the host.

The lysosome contains hydrolytic enzymes that break down biological materials. If these enzymes were released, they could cause cell death by autolysis.

The inactivation of a transport protein would not be too catastrophic, and would not lead to cell death. Overstimulation of the cell cycle would lead to increased mitosis and cell proliferation, the opposite of cell death. Eventually, this overstimulation may be detected and cause apoptosis, but it will not directly cause the cell death. A silent mutation would not alter the protein created from the gene, and thus would have no effect on the cell.