Opalescence in Australian-grown pecan kernels: Occurrence and causes

Opalescence is an unattractive browning of the interior of the pecan kernel compared to the white interior of normal kernels. The discoloration is due to the presence of free oil, resulting from decompartmentalization in the endosperm of opalescent,pecans. Using a subjective scoring system, approximately 70% of Australian-grown pecan kernels tested were found to exhibit opalescence to some degree. Evaluation of kernels for opalescence during the harvesting-processing chain showed that opalescence first becomes evident in kernels after mechanical cracking. Opalescent kernels were found to have lower levels of calcium and higher amounts of oil compared to nonoptalescent kernels. Differential scanning calorimetry showed that kernels do not freeze at -18 degreesC

Loss of function of the carbon catabolite repressor CreA leads to low but inducer‐independent expression from the feruloyl esterase B promoter in Aspergillus niger

OBJECTIVE: With the aim to decipher the mechanisms involved in the transcriptional regulation of feruloyl esterase encoded by faeB, a genetic screen was performed to isolate A. niger mutants displaying inducer-independent expression from the faeB promoter. RESULT: PfaeB-amdS and PfaeB-lux dual reporter strains were constructed and used to isolate trans-acting mutants in which the expression of both reporters was increased, based on the ability to grow on acetamide plates and higher luciferase activity, respectively. The genetic screen on the non-inducing carbon source D-fructose yielded in total 111 trans-acting mutants. The genome of one of the mutants was sequenced and revealed several SNPs, including a point mutation in the creA gene encoding a transcription factor known to be involved in carbon catabolite repression. Subsequently, all mutants were analyzed for defects in carbon catabolite repression by determining sensitivity towards allyl alcohol. All except four of the 111 mutants were sensitive to allyl alcohol, indicating that the vast majority of the mutants are defective in carbon catabolite repression. The creA gene of 32 allyl alcohol sensitive mutants was sequenced and 27 of them indeed contained a mutation in the creA gene. Targeted deletion of creA in the reporter strain confirmed that the loss of CreA results in constitutive expression from the faeB promoter. CONCLUSION: Loss of function of CreA leads to low but inducer-independent expression from the faeB promoter in A. niger. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s10529-021-03104-2