A component of the septation initiation network complex, AaSepM, is involved in multiple cellulose-responsive signaling pathways in Aspergillus aculeatus

Abstract To elucidate the regulatory mechanisms of various cellulolytic enzyme genes in Aspergillus aculeatus , we identified one mutant that reduced the expression of FIII-avicelase ( chbI ) in response to cellulose from 12,000 A . aculeatus T-DNA-inserted mutants. The T-DNA inserted into a putative protein kinase gene similar to AN10082 in A . nidulans , the serine–arginine protein kinase F, SrpkF. The fold increase in srpkF gene expression in response to various carbon sources was 2.3 (D-xylose), 44 (Avicel®), 59 (Bacto™ Tryptone), and 98 (no carbon) compared with D-glucose. The deletion of srpkF in A . aculeatus resulted in a significant reduction in the cellulose-responsive expression of chbI , hydrocellulase ( cel7b ), and FIb-xylanase ( xynIb ) genes at an early induction phase. However, the srpkF deletion did not affect the expression of xynIb in response to D-xylose. Furthermore, the srpkF -overexpressing strain that expresses the srpkF gene at levels from four- to nine-fold higher than the control strain stimulated the expression of cbhI and cel7b in response to cellobiose and the FI-carboxymethyl cellulase gene ( cmc1 ) and xynIb in response to xylose. The expression of cbhI and cel7b is regulated by a transcriptional activator, ManR, and the expression of cmc1 and xynIb is regulated by XlnR. Our data demonstrate that SrpkF can stimulate both the ManR- and XlnR-dependent signaling pathways in response to cellobiose and D-xylose in A . aculeatus .

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A compendium of G-protein–coupled receptors and cyclic nucleotide regulation of adipose tissue metabolism and energy expenditure

Clinical Science ◽

10.1042/cs20190579 ◽

2020 ◽

Vol 134 (5) ◽

pp. 473-512 ◽

Cited By ~ 5

Author(s):

Ryan P. Ceddia ◽

Sheila Collins

Keyword(s):

Adipose Tissue ◽

Energy Expenditure ◽

Signaling Pathways ◽

G Protein ◽

Uncoupling Protein ◽

Beige Adipocytes ◽

Nucleotide Regulation ◽

Ucp1 Expression ◽

Thermogenic Adipocytes ◽

G Protein Coupled

Abstract With the ever-increasing burden of obesity and Type 2 diabetes, it is generally acknowledged that there remains a need for developing new therapeutics. One potential mechanism to combat obesity is to raise energy expenditure via increasing the amount of uncoupled respiration from the mitochondria-rich brown and beige adipocytes. With the recent appreciation of thermogenic adipocytes in humans, much effort is being made to elucidate the signaling pathways that regulate the browning of adipose tissue. In this review, we focus on the ligand–receptor signaling pathways that influence the cyclic nucleotides, cAMP and cGMP, in adipocytes. We chose to focus on G-protein–coupled receptor (GPCR), guanylyl cyclase and phosphodiesterase regulation of adipocytes because they are the targets of a large proportion of all currently available therapeutics. Furthermore, there is a large overlap in their signaling pathways, as signaling events that raise cAMP or cGMP generally increase adipocyte lipolysis and cause changes that are commonly referred to as browning: increasing mitochondrial biogenesis, uncoupling protein 1 (UCP1) expression and respiration.

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