In response to stress certain genes are induced. These genes are induced due to some transcription factors (TFs). So how are these particular TFs transcribed in response to that particular stress? Just trying to better understand things. If anyone can give me a good reference, will be thankful.
Hi Brijesh,
One of the best examples answering your question is given in the survey of F. Estruch published in FEMS Microbiol Rev. 2000 24:469-86 entitled “Stress-controlled transcription factors, stress-induced genes and stress tolerance in budding yeast”. Abstract: The transcriptional response to environmental changes is a major topic in both basic and applied research. From a basic point of view, to understand this response includes unravelling how the stress signal is sensed and transduced to the nucleus, to identify which genes are induced under each stress condition and, finally, to establish the phenotypic consequences of this induction in stress tolerance. The possibility of using genetic approaches has made the yeast Saccharomyces cerevisiae a compelling model to study stress response at a molecular level. Moreover, this information can be used to isolate and characterize stress-related proteins in higher eukaryotes and to design strategies to increase stress resistance in organisms of industrial interest. In this review the progress made in recent years is discussed.
Best wishes,
Ilya
Hello Brijesh,
In vertebrates, glucocorticoids (GC) are probably the most well studied hormones that, among other things, increase in response to a stressor. GCs bind with glucocorticoid receptors (GRs) on cell surfaces. This complex translocates to the nucleus where it acts as a transcription factor (TF) to increase or decrease gene expression. It can up-regulate or repress the expression of other TFs that have various actions, including ones that are anti- and pro-inflammatory. GCs are steroid hormones enzematically synthesized from cholesterol, so they are not produce directly via transcription. I am no expert on the mechanistic side of stress physiology, but a quick search for "glucocorticoid transcription factor" produced a number of papers that look like would be good starting points (e.g., http://www.ncbi.nlm.nih.gov/pubmed/11448148).
Best,
Blake
All organisms need to sense and respond to conditions that stress their homeostatic mechanisms. The cellular response to stress represents an adaptation to environmental variables, such as nutrient supply, temperature or oxidative stress. This response to extra- or intracellular stress is accompanied by marked alterations of gene expression. Stress stimuli have been traditionally shown to activate members of mitogen-activated protein kinases (MAPKs), including BMK/ERK5, the 38-kDa protein kinases (p38 MAPKs) and the c-Jun NH2-terminal protein kinases (JNKs). JNKs belong to stress-activated protein kinases (SAPKs) that play a crucial role in the cellular response to environmental stress and balance prosurvival stimuli with opposing signals leading to apoptosis (Schreiber et al. 1995; Chen et al. 1996). The activity of JNKs is stimulated by exposure to UV-B radiation, alkylating agents, hyperosmotic shock, proinflammatory cytokines, and oxidative damage (Martindale and Holbrook 2002). Anisomycin, a widely used inducer of all SAPKs, inhibits eukaryotic peptidyl transferase and activates JNKs through an ill-defined ribosome-dependent mechanism (Iordanov et al. 1997). Upon activation, JNKs phosphorylate various target proteins, such as cJun, ATF-2, and Elk-1, to alter their activity and elicit biological effects. The activity of JNK is regulated through phosphorylation on threonine and tyrosine residues in the T*PY* motif by SEK1/MKK4 (Derijard et al.1995), which in turn is activated by upstream kinases, e.g., MEKK-1 and ASK (Barr and Bogoyevitch 2001).
All mechanisms that affect a cell’s temporal need for protein biosynthesis depend and impinge on the availability of ribosomes and its constituents. Therefore, transcription of rRNA genes by RNA polymerase I (Pol I) is highly regulated to be responsive to both general metabolism and specific environmental challenges (for review,see Grummt 2003; Moss 2004). The key player in growth-dependent regulation of rDNA transcription is the transcription initiation factor TIF-IA, the mammalian homolog of yeast Rrn3p (Bodem et al. 2000; Moorefield et al. 2000) that is associated with a subpopulation of Pol I (Tower and Sollner-Webb 1987; Schnapp et al. 1993). TIF-IA interacts with the TBP-containing factor TIF-IB/SL1, thereby targeting Pol I to the rDNA promoter (Miller et al. 2001; Cavanaugh et al. 2002; Yuan et al. 2002). Importantly, the amount of Rrn3p/TIF-IA associated with Pol I, but not the overall level of Rrn3p/ TIF-IA, is decreased in stationary yeast (Milkereit and Tschochner 1998) and starved or cycloheximide-treated mammalian cells 2002) indicating that transcriptional shut-off is caused
by dissociation of TIF-IA from Pol I. These and other experiments demonstrate that most, if not all, growth dependent control of rDNA transcription may be exerted by the formation and recruitment of TIF-IA/Pol I complexes to the rDNA promoter. In support of TIF-IA playing a central role in modulating Pol I transcription in response to external signals, TIF-IA is phosphorylated at multiple sites and both the phosphorylation pattern and the activity of TIF-IA is altered in response to environmental changes. Conditions that support growth and proliferation, such as nutrient and growth factor availability, trigger signaling pathways that activate TIF-IAby phosphorylation of serine residues 44, 633, and 649 by mTOR- and MAPK-dependent signaling cascades (Zhao et al. 2003; Mayer et al. 2004).
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