The signaling system with chemokines and cytokines is an example of a paracrine signaling process, where nearby cells communicate with each other, rather than autocrine signaling, where a single cell releases a signal to itself. The attraction of macrophages to the site of infection must occur quickly, much faster than several days or weeks. It also must use a second messenger, which will likely have immediate cytosolic effects as well as effects on genetic expression, because it acts through a surface receptor on the macrophage.

Paracrine signaling is the communication between neighboring cells, such as the process described in the question. Autocrine signaling is the use of chemical mediators to activate the same cell that secreted the mediator. Endocrine signaling is the use of chemical mediators to communicate with distant cell targets.

Isotype is not a form of signal, and refers to similar structures. Autologous tissues refer to tissues taken from the same individual, and is also not a form of signaling.

Signal transduction involves transmission of signals between cells. In a normal signal transduction pathway, a ligand (such as a hormone and neurotransmitter) binds to a cell membrane receptor on the extracellular side. Ligand binding initiates a response on the intracellular side. One such response includes the binding of the intracellular side to an effector protein. Binding of the receptor to an effector protein releases second messenger molecules that propagate and amplify the signal, often influencing transcription factors and gene expression.

There are several signal transduction pathways, but the ligand always binds to the extracellular side of the receptor and initiates a response on the intracellular side of the receptor.

A transmembrane receptor, by definition, is a molecule that is inserted into a membrane (such as the plasma membrane of the cell). Recall that a membrane found in a cell is made up of a phospholipid bilayer, which contains both hydrophobic (nonpolar) and hydrophilic (polar) regions. The hydrophobic regions are found on the inside and the hydrophilic regions are found facing either the cytoplasm or the extracellular space.

To insert into a phospholipid bilayer, transmembrane receptors must have both hydrophobic and hydrophilic regions. The hydrophobic portion of the receptor is found inside the hydrophobic core of the membrane and the hydrophilic iregion s found facing the cytoplasm or extracellular space. A ligand typically contacts a transmembrane receptor from the outside or from the cytoplasm; therefore, the ligand typically binds to the hydrophilic portion of the receptor.

The question states that the type III secretion system involves a bacterium making contact with a nearby host cell. Recall that if a cell makes contact with the nearby cell for signal transduction, then the signal is characterized as a juxtacrine signal. In paracrine signaling, on the other hand, the signaling cell secretes a chemical signal such as a neurotransmitter. This chemical binds to receptors on a nearby cell and transmits the signal; in paracrine signaling the two cells never come in contact.

Endocrine signaling involves release of a chemical hormone that enters the bloodstream and signals cells elsewhere in the body. Autocrine signaling involves a cell releasing a molecule that binds to receptors on its own surface; therefore, in autocrine signaling the signaling cell and the target cell are the same.

A transmembrane receptor is any receptor that inserts itself into a membrane. A cell has a phospholipid bilayer membrane surrounding most of the organelles and the cell itself (the plasma membrane). Transmembrane receptors can be found on all of these membranes because the receptors are essential for receiving signals from the outside environment; therefore, you can find transmembrane receptors on the plasma membrane and on the nuclear membrane. Statement I is true.

A prototypical receptor has a ligand-binding site. Once the ligand binds, the receptor signals the cell accordingly. This signal induction can occur via several ways. One way is for a receptor itself to be an ion channel; upon ligand binding the channel opens and transports ions across the plasma membrane, which induces a signal inside the cell. Another way is for a receptor to be a G protein coupled receptor, which induces a signaling cascade that leads to the activation of the second messenger signaling molecule cAMP. There are several ways receptors can induce a signal; therefore, not all receptors are ion channels. Statement II is false.

A ligand can be either polar or nonpolar. The classic example is hormones. Recall that there are both polar and nonpolar (steroid) hormones. Polar hormones, such as the ones released from the pituitary, can’t traverse the hydrophobic core of the phospholipid bilayer; therefore, their receptors are found on the plasma membrane. Steroid hormones, released from the adrenal glands and gonads, can pass through the hydrophobic core and enter the cell. Upon entering the cell, the steroid hormone binds to receptors in the cytoplasm or on the nuclear membrane. Statement III is true.

To answer this question you need to know the difference between a first and a second messenger molecule. First messenger molecules are extracellular molecules such as peptide hormones that bind to the receptor and induce a signal. Second messenger molecules, however, are intracellular molecules that are released and activated by first messenger molecules. cAMP is an intracellular molecule that is activated by signaling from a G-protein coupled receptor; therefore, it is a second messenger molecule. cAMP plays an important role in activation of several signal transduction pathways.

An extracellular signal needs to be amplified by the cell so that the signal reaches all of the target regions. Second messenger molecules, such as cAMP, play an important role in this amplification.

Eukaryotic cells contain mitochondria. The inner membrane of the mitochondrion houses ATP synthase proteins, which generate molecular energy via oxidative phosphorylation. This is the primary source of cellular energy in the form of ATP.

Chloroplasts are another eukaryotic organelle involved in energy production. However, the primary function of the chloroplast is to use light energy to generate glucose from carbon dioxide. This glucose is then metabolized via cellular respiration, utilizing the mitochondria for the majority of ATP synthesis.

This question asks how the response of muscle of an MG patient would differ from the response of muscle of a healthy person to stimulation by a neuron. This is a question that can stand alone from the passage; no information or data from the passage is required to answer the question.

When acetylcholine binds its receptor on a muscle cell it produces a depolarization wave that opens  channels in the plasma membrane and sarcoplasmic reticulum. As a result,  flows out into the sarcoplasm where it stimulates the interaction of actin and myosin and the sliding of the filaments. Since a patient with myasthenia gravis will have a reduced number of functional acetylcholine receptors, the depolarization signal will be smaller, less  will be released and fewer actin-myosin cross bridges will form. This sequence of events will result in the weaker contraction in the muscle of the myasthenia gravis patient. The number of troponin molecules bound to tropomyosin does not change during contraction. Troponin is bound to tropomyosin when the muscle is at rest. When  is released from the sarcoplasmic reticulum, it binds to troponin and causes it to twist the tropomyosin enough to expose the actin myosin binding sites. Since troponin is bound to tropomyosin at rest and during contraction, there shouldn’t be any difference in the number of troponin-tropomyosin interactions in patients with myasthenia gravis as compared with normal individuals.

During a severe asthma attack, one should administer cpinephrine. Epinephrine binds to the beta-2 receptor. As mentioned in the passage, the activation of the beta-2 receptor will activate intercellular level of cyclic AMP. Cyclic AMP will then activate protein kinase A, which will then phosphorylate various proteins. Therefore, we want to increase cAMP levels, adenylate cyclase activity and decrease phospholipase C activity.