Leaf economics and hydraulic traits are critical to leaf photosynthesis, yet it is debated whether these two sets of traits vary in a fully coordinated manner or there is room for independent variation. Here, we tested the relationship between leaf economics traits, including leaf nitrogen concentration and leaf dry mass per area, and leaf hydraulic traits including stomatal density and vein density in five tropical-subtropical forests. Surprisingly, these two suites of traits were statistically decoupled. This decoupling suggests that independent trait dimensions exist within a leaf, with leaf economics dimension corresponding to light capture and tissue longevity, and the hydraulic dimension to water-use and leaf temperature maintenance. Clearly, leaf economics and hydraulic traits can vary independently, thus allowing for more possible plant trait combinations. Compared with a single trait dimension, multiple trait dimensions may better enable species adaptations to multifarious niche dimensions, promote diverse plant strategies and facilitate species coexistence.

Dynamic changes in transcription factor function can be mediated by switching its interaction with coactivators and corepressors. Erythroid Krüppel-like factor (EKLF) is an erythroid cell-specific transcription factor that plays a critical role in ␤-globin gene activation via its interactions with CBP/p300 and SWI/SNF proteins. Unexpectedly, it also interacts with Sin3A and histone deacetylase 1 (HDAC1) corepressors via its zinc finger domain. We now find that selected point mutants can uncouple activation and repression and that an intact finger structure is not required for interactions with Sin3A/HDAC1 or for transrepression. Most intriguingly, EKLF repression exhibits stage specificity, with reversible EKLF-Sin3A interactions playing a key role in this process. Finally, we have located a key lysine residue that is both a substrate for CBP acetylation and required for Sin3A interaction. These data suggest a model whereby the stage of the erythroid cell alters the acetylation status of EKLF and plays a critical role in directing its coactivator-corepressor interactions and downstream transcriptional effects.A pivotal control point for the regulation of gene expression is at the initial generation of the transcript (8, 46). The eukaryotic cell has developed a wide range of control within which a gene can be activated from a dormant state or repressed from an activated state (59). These states can be temporally fixed by the additional controls imposed by chromatin structure and epigenetic marks upon both histones and DNA (60). Proteins that impose such determinants have been generally segregated into transcriptional activators and repressors (37). However, a recent realization that adds an additional layer of complexity is that such a demarcation of function is oversimplified, as some factors can do double duty as activators and repressors (3,20,21). These activities are controlled by a variety of external stimuli and provide a means by which the surprisingly low number of genes in the mammalian genome can exert multiple effects on genomic targets (33).Erythroid Krüppel-like factor (EKLF/KLF1) controls adult ␤-globin gene expression by the interaction of its three zinc fingers with the CAC element (5ЈCCACACCCT3Ј) located within the proximal promoter (4,40,48). Genetic ablation of EKLF leads to loss of the DNase-hypersensitive site at the ␤-promoter and absence of ␤-globin gene expression, resulting in embryonic lethality due to a profound ␤-thalassemia and toxic accumulation of ␣-globin chains (34,44,50,63). Murine yolk sac (primitive) erythroid cells express embryonic ␤-like globins and appear normal, but the lethality arises at the time of the switch to adult ␤-globin expression, which in the mouse occurs in the definitive erythroid cells of the fetal liver (58). EKLF's ability to interact with p300/CBP (67) and with the SWI/SNF complex (2) suggests a means by which EKLF integrates these components at the ␤-promoter and induces transcription initiation. These interactions are interrelated, as p300/CBP acetylat...

Porcine epidemic diarrhea virus (PEDV) is a globally distributed alphacoronavirus that has re-emerged lately, resulting in large economic losses. During viral infection, interferon (IFN-I) plays a vital role in the antiviral innate immunity. However, PEDV has evolved strategies to limit IFN-I production. To suppress virus replication, the host must activate the IFN-stimulated genes and some host restriction factors to circumvent viral replication. This study observed that PEDV infection-induced early growth response gene 1 (EGR1) expression in PEDV-permissive cells. EGR1 overexpression remarkably suppressed PEDV replication. In contrast, depletion of EGR1 led to a significant increase in viral replication. EGR1 suppressed PEDV replication by directly binding to the IFN-regulated antiviral (IRAV) promoter and upregulating IRAV expression. A detailed analysis revealed that IRAV interacts and colocalizes with the PEDV nucleocapsid (N) protein, inducing N protein degradation via E3 ubiquitin ligase MARCH8 to catalyze N protein ubiquitination. Knockdown of endogenous MARCH8 significantly reversed IRAV-mediated N protein degradation. The collective findings demonstrate a new mechanism of EGR1-mediated viral restriction, in which EGR1 upregulates the expression of IRAV to degrade PEDV N protein through MARCH8. IMPORTANCE PEDV is a highly contagious enteric coronavirus that has rapidly emerged worldwide and caused severe economic losses. No currently available drugs or vaccines could effectively control PEDV. PEDV has evolved many strategies to limit IFN-1 production. We identified EGR1 as a novel host restriction factor and demonstrated that EGR1 suppresses PEDV replication by directly binding to the IRAV promoter and upregulating the expression of IRAV, which interacts and degrades the PEDV N protein via E3 ubiquitin ligase MARCH8 to catalyze nucleocapsid protein ubiquitination, which adds another layer of complexity to innate antiviral immunity of this newly identified restriction factor. A better understanding of the innate immune response to PEDV infection will aid the development of novel therapeutic targets and more effective vaccines against virus infection.

Emerging coronaviruses (CoVs) can cause severe diseases in humans and animals, but none of the currently available drugs or vaccines can effectively control these diseases. During viral infection, the host will activate the interferon (IFN) signaling pathways and host restriction factors in maintaining the innate antiviral responses and suppressing viral replication.