In this week's PNAS Early Edition, investigators at the University of California, Irvine, and at Metabolon discuss their analysis of "a comprehensive dataset of over 500 metabolites identified by mass spectrometry," which, through computational modeling, helped them to uncover "evidence of synergistic nodes between the circadian transcriptome and specific metabolic pathways." The public-private team presents an integrated map that it says "illustrates the coherence within the circadian metabolome, transcriptome, and proteome and how these are connected through specific nodes that operate in concert to achieve metabolic homeostasis."
Researchers at the University of Texas at Austin and at the University of Cambridge this week show that, in the endosperm of Arabidopsis seeds, "p4-siRNA accumulation depends on the maternal genome dosage," and that "maternal p4-siRNAs target transposable elements and TE [transposable element]-associated genes in seeds." Overall, the researchers say that their study provides "unique genetic evidence for maternal siRNAs in response to parental genome imbalance and in control of transposons and gene expression during endosperm development."
Elsewhere in this week's Early Edition, an international team led by investigators at the University of California, Los Angeles, presents a "genome-wide analysis of histone H3.1 and H3.3 variants in Arabidopsis thaliana." The team says the results of its analysis are "broadly consistent with the hypothesis that H3.1 acts as the canonical histone that is incorporated during DNA replication, whereas H3.3 acts as the replacement histone that can be incorporated outside of S-phase during chromatin-disrupting processes like transcription."
Ohio State University's Carlo Croce and his colleagues discuss feedback circuitry among the microRNAs miR-25 and miR-32 and the TP53 tumor suppressor gene, and how that plays a role in glioblastoma multiforme. In their PNAS paper published online in advance this week, Croce et al. report results that "define miR-25 and -32 as positive regulators of p53, underscoring their role in tumorigenesis in glioblastoma."