## 1 Introduction  
Citrus canker, caused by the bacterium _Xanthomonas citri_ subsp. _citri_ is one of the most devastating diseases found in citrus-growing areas [1; 2]. Despite successful eradication programs in Florida (USA) [3] and Sao Paulo (Brazil) [2], these two major orange producers in the world face constant citrus canker epidemics [4; 5]. For different reasons, both eradication programs were halted in Brazil and Florida [6]; hence, the citrus canker has increased substantially in these areas, and now growers are expected to live with this disease endemically [2]. There is no cure, and chemical control is limited to the application of cupric compounds [4; 7], which also have limited effectiveness [8]. Therefore, strict management practices are essential to keep field levels of _X. citri_ at low levels [2; 5]. _X. citri_ is a biotrophic phytopathogen [9] and, as such, relies entirely on its plant host to survive. It infects all citrus varieties, which have different levels of susceptibility [10]. _X. citri_ has limited survival outside of the citrus plant, does not utilize insect vectors or an alternate host, so dissemination is via wind-blown water droplets, which carry the bacterium that oozes from canker lesions. In addition, human and tool movements between infected and healthy orchards are important mechanisms for bacteria spreading [1; 3]. Despite its relatively simple life cycle, citrus canker outbreaks are recurrent, meaning current efforts to suppress dissemination are not very effective. Therefore, it is imperative to better understand _X. citri_ survival after the use of cupric bacteriides to design more sustainable management practices to decrease the environmental and economic damage caused by the disease in the field. _X. citri_, like most bacteria, survive most adverse conditions. Nutrient deprivation, heat and cold stresses, as well as a myriad of dangerous chemicals, like antibiotics, are examples of challenges microorganisms face continuously. Hence, strains are selected to withstand these adverse conditions, primarily through genetic mutation and/or the introduction of foreign genetic material (like plasmids), which allow cells to survive under otherwise prohibitive conditions. Once acquired, the resistance genes are stably passed to offspring, giving rise to resistant strains. However, another widespread survival mechanism is the persistence phenotype. Characterized by a general suppression of bacterial metabolism, this dormancy phenomenon was first described in the 1940s [11; 12], when a small subpopulation of _Staphylococcus aureus_ cells entered into a dormant state, protecting them from the antibiotic. Later, reports presented a so-called \"viable, but non-culturable\" state (\"VBNC\") in _Escherichia coli_ and _Vibrio cholerae_[13], which was further described in many other bacterial species. Some inconsistencies in the nomenclature of these \"dormant\" phenotypes have occurred in the following years. Recent works have clarified the nature of persistence, showing that, at least for _E. coli_, the viable cells in the VBNC state are persister cells [14] and that persistence stems from ribosome dimerization [15]. In addition, advances in the resuscitation of persisters using single-cell microscopy have shown that they wake in a heterogeneous manner when exposed to carbon sources (rather than spontaneously) based on their ribosome content [16] and that specific chemicals can wake/resuscitate different bacterial strains [17; 18]. Notably, when persisters resuscitate, they grow at the same growth rate as the wild-type strain [14]. The basic principle behind persistence is that many antimicrobials rely on active metabolic pathways [19]; consequently, by a general metabolic arrest, these chemicals do not find their targets and do not harm the dormant cells. The occurrence of persistence seems to be ubiquitous among bacteria, under both nutrient and antibiotic stress conditions. Even archaea become persisters [20].