MeaB-dependent nutrition sensing regulates autolysis in carbon starved Aspergillus nidulans cultures

Abstract

Carbon starvation induced autolysis is an active process of self-digestion and is under complex regulation in Aspergillus nidulans. In this study we investigated how autolysis depends on the composition of the culture medium, especially on the presence of yeast extract. We demonstrated that the rate of autolytic cell wall degradation as well as the extracellular chitinase and proteinase productionsThe effect of yeast extract on carbon starved cultures was independent of loss-of-function mutations in the carbon and nitrogen regulatory genes creA and areA and in the heterotrimeric G protein signalling genes fadA and ganB. In contrast, the nitrogen regulating transcription factor MeaB was involved in the yeast-extract-mediated repression of autolysis. Reverse transcriptase -polymerase chain reaction (RT-PCR) experiments demonstrated that MeaB affects the FluG-BrlA sporulation regulatory pathway by affecting transcription of brlA, a gene also initiating the autolytic cell wall degradation in this fungus.Keywords MeaB · Aspergillus nidulans · Autolysis · Carbon starvation · Chitinase digestion of ageing hyphal cultures, occurring as a result of hydrolase activity and causing vacuolization and disruption of cell organelles and cell wall structures [1]. Autolysis regulated process, which helps these microorganisms to survive in a continuously changing, hostile environment [2][3][4]. Emerging regulatory elements of autolysis provide us with promising tools to control and manipulate this process for several practical purposes in the fermentation industry [2,4]. Moreover, a deeper understanding of the underlying mechanism of fungal autolysis may also be exploited in future antifungal drug research [5][6][7]. Aspergillus nidulans, the last step of carbon starvation triggered autolysis is the degradation of the cell wall of empty hyphae (autolytic cell wall degradation). The regulation of this process is independent of concomitantly progressing cell death [4]. In previous experiments, we studied the glucose-mediated repression of autolysis in A. nidulans. We found that glucose repressed the autolytic cell wall degradation via the carbon catabolite repressor CreA as well as independently of CreA, via repressing the conidiogenesis regulatory gene brlA and activating the heterotrimeric G protein FadA-dependent signalling [4, 8].Here, we studied the effect of yeast extract on the autolysis of A. nidulans. We demonstrated that the bZip-type transcription factor MeaB, an activator of nmrA expression and a co-repressor of areA expression [9], was involved in the yeast-extract-mediated repression of autolytic cell wall degradation.A. nidulans FGSC 24 (sC12), FGSC 26 (biA1, veA1), FGSC 41 (biA1, sB3), FGSC 451 (pabaA1, meaB6, cnxH3, sC12), FGSC 553 (biA1, cnxH3) and FGSC 1056 (yA2,

The extracellular β-1,3-endoglucanase EngA is involved in autolysis of Aspergillus nidulans

“…b-1,3-glucans and chitin (Fontaine et al 2000;Bernard and Latgé 2001), requires the concerted and highly organized action of a wide array of hydrolases (Adams 2004). The absent or decreased activity of one key element in cell wall hydrolysis may result in an overall decrease in the liberation of cell wall monomers (sugars, amino acids), which are of cardinal importance in the satisfactory induction of these enzymes (Pitson et al 1993;Pusztahelyi et al 2006;Martin et al 2007;Szilágyi et al 2010). An unbalanced hydrolase production would obviously lead to inefficient biopolymer degradation and the dissipation of the available nutrient and energy resources, which are rather limited under carbon starvation (McIntyre et al 1999;Emri et al 2004).…”

Extracellular proteinase formation in carbon starving Aspergillus nidulans cultures – physiological function and regulation

“…Proteinase formation in autolytic A. nidulans cultures was also influenced by CreA dependent and CreA independent carbon metabolite repressions (Tables 3 and 4 [16]). Furthermore, a mutation in meaB nitrogen metabolite repressor transcription factor delayed the repressive effect of sodium glutamate (Table 4 [40]). However, these effects were less significant in comparison to FluG-BrlA or pH dependent regulations.…”