Disease relevance of TotA

• TotA is strongly induced upon bacterial challenge, as well as by other types of stress such as high temperature, mechanical pressure, dehydration, UV irradiation, and oxidative agents [1].
• All Tot genes are induced under stressful conditions such as bacterial infection, heat shock, paraquat feeding or exposure to ultraviolet light, suggesting that all members of this family play a role in Drosophila stress tolerance [2].

High impact information on TotA

• We present the JAK/STAT-dependent humoral factors, such as the thioester-containing proteins and the Tot peptides, produced by the fat body in response to septic injury [3].
• Although TotA is only induced by severe stress, it responds to a much wider range of stimuli than heat shock genes such as hsp70 or immune genes such as Cecropin A1 [1].
• The Turandot A (TotA) gene encodes a humoral factor, which is secreted from the fat body and accumulates in the body fluids [1].
• The MAPKKK Mekk1 regulates the expression of Turandot stress genes in response to septic injury in Drosophila [4].
• Our analysis indicates that Tot genes show a complex regulation pattern including signals from both the JAK-STAT and Imd pathways and Mekk1 [4].

Biological context of TotA

• Here we show that TotA belongs to a family of eight Tot genes distributed at three different sites in the Drosophila genome [2].
• The induction of the Tot genes differs in important respects from the heat shock response, such as the strong but delayed response to bacterial infection seen for several of the genes [2].

Analytical, diagnostic and therapeutic context of TotA

• Using oligonucleotide microarrays, we now demonstrate that the MAPKKK Mekk1 regulates a small subset of genes induced by septic injury including Turandot (Tot) stress genes [4].

References