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Felton, A.

Publications and source records attributed to Felton, A..

2 recordsLinked to original sources

What happens to oak growth and survival when there is both competition and browsing?

Competition from neighboring vegetation and browsing by large herbivores are two of the most important factors affecting the structure and dynamics of temperate forests. While the previous literature has been able to identify individual negative effects from competition or browsing, no one has yet identified and quantified both the individual and the joint effects. Still, when plants face both competition and browsing, it is possible that the combined effect is not simply a sum of the individual negative effects, but perhaps a more complicated situation, where plants perform either better (in case there is also a facilitative effect from the neighboring vegetation) or worse (if the effects amplify each other) than they would if experiencing only one of the two factors. In this paper, we focus on regeneration of oak (Quercus robur L) to study these questions. We analyze a rich data set from a large long-term field experiment conducted at multiple sites in mixed temperate forests in southern Sweden over almost a decade. By the use of four separate treatments on each site - (i) neither competition, nor browsing, (ii) only competition, (iii) only browsing, and (iv) both competition and browsing - we can identify and quantify both the individual and combined effects of competition and browsing on oak growth and survival. We find that both competition and browsing individually affect growth and survival negatively. For growth, browsing has the largest effect, while competition is the larger problem from a survival point of view. When the plant experiences both competition and browsing, the combined, negative, effect is larger than either individual effect for survival, but for growth, the relationship is more complicated, and the surrounding woody vegetation offers at least some protection for the oak, reducing the negative effects from browsing.

ecology

TRIM34 acts with TRIM5 to restrict HIV and SIV capsids

The HIV-1 capsid protein makes up the core of the virion and plays a critical role in early steps of HIV replication. Due to its exposure in the cytoplasm after entry, HIV capsid is a target for host cell factors that act directly to block infection such as TRIM5 and MxB. Several host proteins also play a role in facilitating infection, including in the protection of HIV-1 capsid from recognition by host cell restriction factors. Through an unbiased screening approach, called HIV-CRISPR, we show that the Cyclophilin A-binding deficient P90A HIV-1 capsid mutant becomes highly-sensitized to TRIM5alpha restriction in IFN-treated cells. Further, the CPSF6-binding deficient, N74D HIV-1 capsid mutant is sensitive to restriction mediated by human TRIM34, a close paralog of the well-characterized HIV restriction factor TRIM5. This restriction occurs at the step of reverse transcription, is independent of interferon stimulation and limits HIV-1 infection in key target cells of HIV infection including CD4+ T cells and monocyte-derived dendritic cells. TRIM34 restriction requires TRIM5alpha as knockout or knockdown of TRIM5alpha results in a loss of antiviral activity. TRIM34 can also restrict some SIV capsids. Through immunofluorescence studies, we show that TRIM34 and TRIM5alpha colocalize to cytoplasmic bodies and are more frequently observed to be associated with infecting N74D capsids than with WT capsids. Our results identify TRIM34 as an HIV-1 CA-targeting restriction factor and highlight the potential role for heteromultimeric TRIM interactions in contributing restriction of HIV-1 infection in human cells.

microbiology