Inhibition of phosphoglucose isomerase allozymes from the wing polymorphic waterstrider, Limnoporus canaliculatus, by pentose shunt metabolites

Abstract

Inhibition of phosphoglucose isomerase (PGI) allozymes from the wing-polymorphic waterstrider, Limnoporus canaliculatus, by three pentose-shunt metabolites was studied at several different temperatures. This was done to determine if the allozymes exhibited a differential ability to participate in lipid biosynthesis via differential partitioning of carbon flux through the pentose shunt versus glycolysis. 6-Phosphogluconate and erythrose-4-phosphate proved to be strong competitive inhibitors of PGI, while sedoheptulose-7-phosphate was a very weak inhibitor. The PGI allozymes from L. canaliculatus were differentially inhibited by 6-phosphogluconate at two of the three temperatures studied. However, this property does not appear to be an adaptive difference between the allozymes but, rather, a correlated effect resulting from variation in substrate binding. Estimates of reaction rates for the allozymes indicate that the differences in inhibition result in no detectable differences in reaction velocities. Thus, no evidence in support of the hypothesis that PGI allozymes from Limnoporus canaliculatus were adapted to function in different metabolic capacities via differential inhibition was obtained in this study. However, the importance of this characteristic in allozymic adaptation in natural populations remains an open question.

Mitonuclear mismatch alters performance and reproductive success in naturally introgressed populations of a montane leaf beetle*

“…1996; Dahlhoff and Rank 2000; Lockwood and Somero 2012). There is also evidence that performance and fitness differences among PGI genotypes are caused by changes in the flow of metabolites through glycolysis (Zera 1987; Staples and Suarez 1997), which subsequently cause differences in energy availability that scale up to ultimately alter physiological, performance and fitness differences between genotypes (Johannesson et al. 1990; Rank and Dahlhoff 2002; Hanski and Saccheri 2006; Dahlhoff et al.…”

“…There is also evidence that performance and fitness differences among PGI genotypes are caused by changes in the flow of metabolites through glycolysis (Zera 1987;Staples and Suarez 1997), which subsequently cause differences in energy availability that scale up to ultimately alter physiological, performance and fitness differences between genotypes (Johannesson et al 1990;Rank and Dahlhoff 2002;Hanski and Saccheri 2006;Dahlhoff et al 2008;Hanski et al 2017). However, conclusive evidence that variation in PGI allozymes is the direct cause of large differences in performance and fitness among variant PGI genotypes remains elusive.…”

Fecundity, growth rate and survivorship at the interface between two contiguous genetically distinct groups of Semibalanus balanoides

“…The relationship between fitness and enzyme activity has been discussed in numerous studies (GPI: Krause 1995, Zera 1987MPI: De La Fuente et al 1986, Hernandez & De La Fuente 1988, see also Schmidt & Rand 1999, and many have related spatial variation in allele frequencies to environmental factors such as temperature (Grant et al 1992), salinity (Theisen 1978), low oxygen concentration (Shihab & Heat 1987) and pollution (heavy metals: Lavie & Nevo 1982, Hvilsom 1983, Nevo et al 1983, Patarnello et al 1991petrochemical agents: Lavie et al 1984). In our experiments, there is no obvious relationship between temperature and the population structure at the GPI* or MPI* loci.…”

Glycolysis and Krebs Cycle Metabolites in Mosquitofish, Gambusia Holbrooki, Girard 1859, Exposed to Mercuric Chloride: Allozyme Genotype Effects

“…The physiological significance of allozyme variation has been studied in relation to thermal adaptation in fishes [12-141 and blue mussel [15], juvenile survival of red deer [ 161, oxygen consumption of a salamander [17], hyperosmotic stress in a copepod [18], and inhibition by metabolic intermediates [19]. In this study, the role of allozymes in the response of mosquitofish to inorganic mercury poisoning was determined by the measurement of glycolysis and Krebs cycle metabolite concentrations, including GPI and MDH substrates.…”