Growth of Salmonella and Other Foodborne Pathogens on Inoculated Inshell Pistachios during Simulated Delays between Hulling and Drying

During harvest, pistachios are hulled, separated in water into floater and sinker streams (in large part on the basis of nut density), and then dried before storage. Higher prevalence and levels of Salmonella were previously observed in floater pistachios, but contributing factors are unclear. To examine the behavior of pathogens on hulled pistachios during simulated drying delays, floater and sinker pistachios collected from commercial processors were inoculated at 1 or 3 log CFU/g with cocktails of Salmonella and in some cases Escherichia coli O157:H7 or Listeria monocytogenes and incubated for up to 30 h at 37°C and 90% relative humidity. Populations were measured by plating onto tryptic soy agar and appropriate selective agars. In most cases, no significant growth (P \u3e 0.05) of Salmonella was observed in the first 3 h after inoculation in hulled floaters and sinkers. Growth of Salmonella was greater on floater pistachios than on corresponding sinkers and on floater pistachios with ≥25% hull adhering to the shell surface than on corresponding floaters with \u3c25% adhering hull. Maximum Salmonella populations (2 to 7 log CFU/g) were ~2-log higher on floaters than on corresponding sinkers. The growth of E. coli O157:H7 and Salmonella on hulled pistachios was similar, but a longer lag time (approximately 11 h) and significantly lower maximum populations (4 versus 5 to 6 log CFU/g; P \u3e 0.05) were predicted for L. monocytogenes. Significant growth of pathogens on hulled pistachios is possible when delays between hulling and drying are longer than 3 h, and pathogen growth is enhanced in the presence of adhering hull material. HIGHLIGHTS • Foodborne pathogens multiplied on undried inshell pistachios. • Pathogen growth was greater when hull material was present. • Drying delays of \u3e 3 h led to significant increases in pathogen populations. • Managing drying delays will reduce the risk for growth of foodborne pathogens

tBRD-1 and tBRD-2 regulate expression of genes necessary for spermatid differentiation

Male germ cell differentiation proceeds to a large extent in the absence of active gene transcription. In Drosophila, hundreds of genes whose proteins are required during post-meiotic spermatid differentiation (spermiogenesis) are transcribed in primary spermatocytes. Transcription of these genes depends on the sequential action of the testis meiotic arrest complex (tMAC), Mediator complex, and testis-specific TFIID (tTFIID) complex. How the action of these protein complexes is coordinated and which other factors are involved in the regulation of transcription in spermatocytes is not well understood. Here, we show that the bromodomain proteins tBRD-1 and tBRD-2 regulate gene expression in primary spermatocytes and share a subset of target genes. The function of tBRD-1 was essential for the sub-cellular localization of endogenous tBRD-2 but dispensable for its protein stability. Our comparison of different microarray data sets showed that in primary spermatocytes, the expression of a defined number of genes depends on the function of the bromodomain proteins tBRD-1 and tBRD-2, the tMAC component Aly, the Mediator component Med22, and the tTAF Sa

Sex-specific chromatin remodelling safeguards transcription in germ cells

Stability of the epigenetic landscape underpins maintenance of the cell-type-specific transcriptional profile. As one of the main repressive epigenetic systems, DNA methylation has been shown to be important for long-term gene silencing; its loss leads to ectopic and aberrant transcription in differentiated cells and cancer1. The developing mouse germ line endures global changes in DNA methylation in the absence of widespread transcriptional activation. Here, using an ultra-low-input native chromatin immunoprecipitation approach, we show that following DNA demethylation the gonadal primordial germ cells undergo remodelling of repressive histone modifications, resulting in a sex-specific signature in mice. We further demonstrate that Polycomb has a central role in transcriptional control in the newly hypomethylated germline genome as the genetic loss of Ezh2 leads to aberrant transcriptional activation, retrotransposon derepression and dramatic loss of developing female germ cells. This sex-specific effect of Ezh2 deletion is explained by the distinct landscape of repressive modifications observed in male and female germ cells. Overall, our study provides insight into the dynamic interplay between repressive chromatin modifications in the context of a developmental reprogramming system