Nutrient sensing
Nutrient sensing is a cell's ability to recognize and respond to fuel substrates such as glucose. Each type of fuel used by the cell requires an alternate pathway of utilization and accessory molecules such as enzymes and cofactors. In order to conserve resources a cell will only produce molecules that it needs at the time. The level and type of fuel that is available to a cell will determine the type of enzymes it needs to express from its genome for utilization. Receptors on the cell membrane's surface designed to be activated in the presence of specific fuel molecules communicate to the cell nucleus via a means of cascading interactions. Nutrient receptors are receptors that are primarily designed to perform the function of nutrient sensing, whereas other receptors are extensively multifunctional and perform many functions besides nutrient sensing. In this way the cell is aware of the available nutrients and is able to produce only the molecules specific to that nutrient type.
Nutrient sensing in mammalian cells
A rapid and efficient response to disturbances in nutrient levels is crucial for the survival of organisms from bacteria to humans. Cells have therefore evolved a host of molecular pathways that can sense nutrient concentrations and quickly regulate gene expression and protein modification to respond to any changes.Cell growth is regulated by coordination of both extracellular nutrients and intracellular metabolite concentrations. AMP-activated kinase (AMPK) and mammalian target of rapamycin complex 1 serve as key molecules that sense cellular energy and nutrients levels, respectively.
- The interplay among nutrients, metabolites, gene expression, and protein modification are involved in the coordination of cell growth with extracellular and intracellular conditions.
Nutrient sensing and epigenetics
Nutrient sensing and signaling is a key regulator of epigenetic machinery in cancer. During glucose shortage, the energy sensor AMPK activates arginine methyltransferase CARM1 and mediates histone H3 hypermethylation, leading to enhanced autophagy. In addition, O-GlcNAc transferase (OGT) signals glucose availability to TET3 and inhibits TET3 by both decreasing its dioxygenase activity and promoting its nuclear export. OGT is also known to directly modify histones with O-GlcNAc. These observations strongly suggest that nutrient signaling directly targets epigenetic enzymes to control epigenetic modifications.Regulation of tissue growth
Nutrient sensing is a key regulator of tissue growth. The main mediator of cellular nutrient sensing is the protein kinase TOR (target of rapamycin). TOR receives information from levels of cellular amino acids and energy, and it regulates the activity of processes involved in cell growth, such as protein synthesis and autophagy. Insulin-like signaling is the main mechanism of systemic nutrient sensing and mediates its growth-regulatory functions largely through the protein kinase pathway. Other nutrition-regulated hormonal mechanisms contribute to growth control of modulating the activity of insulin-like signaling.Nutrient sensing in plants
Higher plants require a number of essential nutrient elements for completing their life cycles. Mineral nutrients are mainly acquired by roots from the rhizosphere and are subsequently distributed to shoots. To overcome with nutrient limitations, plants have evolved a set of elaborate responses consisting of sensing mechanisms and signaling processes to perceive and adapt to external nutrient availability.Plants obtain most necessary nutrients by taking them up from the soil into their roots. Although plants cannot move to a new environment when nutrient availability is less than favorable, they can modify their development to favor root colonization of soil areas where nutrients are abundant. Therefore, plants perceive the availability of external nutrients, like nitrogen, and couple this nutrient sensing to an appropriate adaptive response.