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Trademark strength, properly understood, refers to the scope of protection afforded a trademark by courts based on: (1) the mark’s tendency to signify to consumers a consistent source of the products to which the mark is affixed; and (2) the mark’s ability to influence a consumer’s purchasing decisions. The stronger the mark, the more uses the mark’s owner may exclude from the marketplace through a trademark infringement or dilution action. Courts typically apply a two-pronged analysis in assessing trademark strength. The court first determines a mark’s inherent strength – the extent to which the mark naturally signals source and drives purchasing decisions. Next, the court inquires into a mark’s actual strength in the marketplace – that is, the mark’s actual tendency to signify source and influence consumers’ purchasing decisions. We argue that the acquired strength prong is insufficiently theorized and lacking in analytical rigor, which results in inconsistent results as judges in each jurisdiction (and indeed, each judge within a jurisdiction) rely on their own peculiar heuristics for determining whether a trademark is strong or weak. Our goal in this article is to develop a better understanding of what is at stake when judges and practitioners think about trademark strength and, additionally, to provide analytical guideposts that judges and practitioners can use that can improve outcomes in two related ways. First, by describing mark strength in a more articulate, consistent manner we can work towards eliminating inconsistency across circuits, thereby promoting more uniform national application of the Lanham Act. Second, by predicting accurately how strong a court will hold a mark to be in litigation, practitioners and markholders can better calculate the risk of bringing suit against an alleged infringer (or diluter).

Gene deletion is one of the most powerful tools to study gene function. In the genomics era there is great demand for fast, simple high-throughput methods for gene deletion to study the roles of the large numbers of genes that are being identified. Here we present an approach that speeds up the process of generation of deletion mutants by greatly simplifying the production of gene deletion constructs. With this purpose we have developed a method, which we named DelsGate (Deletion via Gateway), that combines PCR and Gateway cloning technology together with the use of the I-SceI homing endonuclease to generate precise deletion constructs in a very simple, universal and robust manner in just 2 days. DelsGate consists of standard PCR of only the 5' and 3' 1 kb gene flanks directly followed by in vitro Gateway cloning and final generation of the circular deletion construct by in vivo recombination in Escherichia coli. For use in DelsGate we have modified a Gateway cloning vector to include selectable markers for the transformation of Ascomycetes and the Basidiomycete fungus Ustilago maydis. The PCR and transformation steps of DelsGate should be well suited for high-throughput approaches to gene deletion construction in fungal species. We describe here the entire process, from the generation of the deletion construct with DelsGate to the analysis of the fungal transformants to test for gene replacement, with the Basidiomycete fungus Ustilago maydis. Application of DelsGate to other fungal species is also underway. Additionally, we describe how this basic approach can be adapted to other genetic manipulations with minor changes. We specifically describe its application to create unmarked deletions in Ralstonia solanacearum, a Gram-negative phytopathogenic bacterium.