Identification and analysis of unitary loss of long-established protein-coding genes in Poaceae shows evidences for biased gene loss and putatively functional transcription of relics

BACKGROUND: Long-established protein-coding genes may lose their coding potential during evolution (“unitary gene loss”). Members of the Poaceae family are a major food source and represent an ideal model clade for plant evolution research. However, the global pattern of unitary gene loss in Poaceae genomes as well as the evolutionary fate of lost genes are still less-investigated and remain largely elusive. RESULTS: Using a locally developed pipeline, we identified 129 unitary gene loss events for long-established protein-coding genes from four representative species of Poaceae, i.e. brachypodium, rice, sorghum and maize. Functional annotation suggested that the lost genes in all or most of Poaceae species are enriched for genes involved in development and response to endogenous stimulus. We also found that 44 mutated genomic loci of lost genes, which we referred as relics, were still actively transcribed, and of which 84% (37 of 44) showed significantly differential expression across different tissues. More interestingly, we found that there were totally five expressed relics may function as competitive endogenous RNA in brachypodium, rice and sorghum genome. CONCLUSIONS: Based on comparative genomics and transcriptome data, we firstly compiled a comprehensive catalogue of unitary gene loss events in Poaceae species and characterized a statistically significant functional preference for these lost genes as well showed the potential of relics functioning as competitive endogenous RNAs in Poaceae genomes. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12862-015-0345-x) contains supplementary material, which is available to authorized users

Improving adaptation to wildfire smoke and extreme heat in frontline communities: evidence from a community-engaged pilot study in the San Francisco Bay Area

Exposure to climate hazards is increasing, and the experiences of frontline communities warrant meaningful and urgent attention towards how to mitigate, manage, and adapt to hazards. We report results from a community-engaged pilot (November 2021–June 2022) of N = 30 participants in four frontline communities of the San Francisco Bay Area, California, USA. The study region is an area where low-income, non-English-speaking residents are inequitably exposed and vulnerable to wildfire smoke, extreme heat, and other climate hazards. Building from a yearslong partnership of researchers, community organizations, and community members, we report the feasibility of a project piloting (1) instruments to monitor indoor air quality, temperature, and participant sleep health, and (2) interventions to improve indoor air quality and support protective behaviors. Data collection included experience-based survey data (via in-person administered surveys and a smartphone application) and interviews about heat and air quality, as well as data from an air monitoring protocol. Results cover the prevalence of hazard exposure and protective actions among participants. We discuss throughout methods for conducting and evaluating a community-engaged pilot, particularly by using a community ambassador program. Implications include the feasibility of community-engaged research projects, including discussion of resources required to accomplish this work

CD4+T Cells in CIKs (CD4+ CIKs) Reversed Resistance to Fas-Mediated Apoptosis Through CD40/CD40L Ligation Rather Than IFN-γ Stimulation

Background: Cytokine-induced killer cells (CIKs) are nonspecific antitumor effectors with superior advantages. CD4+ CIKs can induce Fas-dependent apoptosis in sensitive Raji cells. Here, a Fas-dependent apoptosis was detected in resistant breast cancer MDA-MB-231 cells, and underlying mechanisms were discriminated. Methods: Amplification of CIKs and purification of CD4+ CIKs were performed in 15 patients with malignant solid tumors. The expression of CD40L and soluble cytokines in CD4+ CIKs were analyzed. The apoptotic rates of tumor cells and the expression of Fas on membranes were detected using flow cytometry assay. The specific blocking antibodies against FasL, CD40L, and interferon-γ (IFN-γ) were added to abolish their effects. The changes of 4 apoptosis-related genes (Bcl-2, Bax, Fas-associating protein with death domain [FADD], and FLICE inhibitory protein [c-FLIP]) in MDA-MB-231 cells cocultured with CD4+ CIKs were measured by real-time quantitative reverse-transcriptase polymerase chain reaction after 6 hours and 24 hours with or without blocking antibodies. Results: Upregulated expression of membrane-attached CD40L and dramatically increased secretion of soluble CD40L and IFN-γ were identified in CD4+ CIK. The susceptibility to Fas-mediated apoptosis of insensitive MDA-MB-231 cells was elevated after being pretreated with supernatants from CD4+ CIK. After coculture with CD4+ CIK, apoptosis in MDA-MB-231 cells paralleled with enhanced expression of Fas was blocked fully by either anti-FasL or anti-CD40L, but only partly by anti-IFN-γ antibodies. The anti-CD40L monoclonal antibody (McAb) rather than anti-IFN-γ McAb induced significant increase of c-FLIP, which negatively correlated with the apoptosis observed in MDA-MB-231 cells. Conclusions: Apoptosis in MDA-MB-231 cells induced by CD4+ CIK is Fas-dependent. The reversion of Fas resistance is mediated through CD40/CD40L ligation rather than IFN-γ stimulation by inhibiting synthesis of c-FLIP