Search for: All records

Contribution: This study examined the role of the engineering and smartness identities of three women as they made decisions about their participation in engineering majors. In addressing the under-representation of women in engineering, particularly in electrical engineering and computer science fields where they have been extremely under-represented, it is important to consider engineering identity as it has been shown to be an important component of major selection and persistence. Background: Smartness is inextricably linked to engineering and prior work has shown that identifying as smart is salient to students who choose engineering majors. However, the relative roles of students’ engineering and smartness identities as they relate to academic decision making and persistence in engineering is not well understood. Research Question: How do engineering identity and smartness identity relate to women’s decisions about choosing engineering majors in the instances of joining engineering, changing engineering major, and leaving engineering? Methodology: Data were collected from a series of three interviews with three different women. Data condensation techniques, including writing participant summary memos and analytic memos, focused on detailing participants’ academic decisions, engineering identity, and smartness identity were used for analysis. Data visualization was used to map the women’s engineering identity and smartness identity to their academic decisions related to their majors. Findings: The findings indicate the participants’ smartness identity was salient in the initial decision to matriculate into engineering, both their engineering and smartness identities remained stable as they persisted in or left engineering. And reveal complex interactions between these identities and decision making. 

H2B mono-ubiquitination (ub1) is an important histone modification attaching a ubiquitin moiety to the small histone H2B and changing the biochemical features of the chromatin. The dynamic equilibrium between H2B ub1 and deubiquitination (deub1) has been shown to affect nucleosome stability, nucleosome reassembly and higher chromatin structure. The above changes mediated by H2B ub1 regulate transcription activation and elongation, and play key roles in multiple molecular and biological processes including growth, development, pathogenesis and aging. In this review, we summarize our current knowledge in regulation of H2B ub1/deub1 equilibrium, and how this modification affects chromatin dynamics and gene expressions. We also discuss the roles of H2B ub1/deub1 cycle in plant-pathogen interactions, and point out the questions that remain to be resolved in future studies.

 

Plant pathogens are challenged by host-derived iron starvation or excess during infection, but the mechanism through which pathogens counteract iron stress is unclear. Here, we found that Fusarium graminearum encounters iron excess during the colonization of wheat heads. Deletion of heme activator protein X (FgHapX), siderophore transcription factor A (FgSreA) or both attenuated virulence. Further, we found that FgHapX activates iron storage under iron excess by promoting histone H2B deubiquitination (H2B deub1) at the promoter of the responsible gene. Meanwhile, FgSreA is shown to inhibit genes mediating iron acquisition during iron excess by facilitating the deposition of histone variant H2A.Z and histone 3 lysine 27 trimethylation (H3K27 me3) at the first nucleosome after the transcription start site. In addition, the monothiol glutaredoxin FgGrx4 is responsible for iron sensing and control of the transcriptional activity of FgHapX and FgSreA via modulation of their enrichment at target genes and recruitment of epigenetic regulators, respectively. Taken together, our findings elucidated the molecular mechanisms for adaptation to iron excess mediated by FgHapX and FgSreA during infection in F. graminearum and provide novel insights into regulation of iron homeostasis at the chromatin level in eukaryotes.

 

Fusarium graminearumproduces the mycotoxin deoxynivalenol (DON) which promotes its expansion during infection on its plant host wheat. Conditional expression of DON production during infection is poorly characterized.

Wheat produces the defense compound putrescine, which induces hypertranscription of DON biosynthetic genes (FgTRIs) and subsequently leads to DON accumulation during infection. Further, the regulatory mechanisms ofFgTRIs hypertranscription upon putrescine treatment were investigated.

The transcription factor FgAreA regulates putrescine‐mediated transcription ofFgTRIs by facilitating the enrichment of histone H2B monoubiquitination (H2B ub1) and histone 3 lysine 4 di‐ and trimethylations (H3K4 me2/3) onFgTRIs. Importantly, a DNA‐binding domain (bZIP) specifically within theFusariumH2B ub1 E3 ligase Bre1 othologs is identified, and the binding of this bZIP domain toFgTRIsdepends on FgAreA‐mediated chromatin rearrangement. Interestingly, H2B ub1 regulates H3K4 me2/3 via the methyltransferase complex COMPASS component FgBre2, which is different fromSaccharomyces cerevisiae.

Taken together, our findings reveal the molecular mechanisms by which host‐generated putrescine induces DON production duringF. graminearuminfection. Our results also provide a novel insight into the role of putrescine during phytopathogen–host interactions and broaden our knowledge of H2B ub1 biogenesis and crosstalk between H2B ub1 and H3K4 me2/3 in eukaryotes.