Soil Biodiversity and Root Pathogens in Agroecosystems

Soil ecosystem is a living and dynamic environment, habitat of thousands of microbial species, animal organisms and plant roots, integrated all of them in the food webs, and performing vital functions like organic matter decomposition and nutrient cycling; soil is also where plant roots productivity represent the main and first trophic level (producers), the beginning of the soil food web and of thousands of biological interactions. Agroecosystems are modified ecosystems by man in which plant, animal and microorganisms biodiversity has been altered, and sometimes decreased to a minimum number of species. Plant diseases, including root diseases caused by soil-borne plant pathogens are important threats to crop yield and they causes relevant economic losses. Soil-borne plant pathogens and the diseases they produce can cause huge losses and even social and environmental changes, for instance the Irish famine caused by Phytophthora infestans (1845–1853), or the harmful ecological alterations in the jarrah forests of Western Australia affected by Phytophthora cinnamomi in the last 100 years. How can a root pathogen species increase its populations densities at epidemic levels? In wild ecosystems usually we expect the soil biodiversity (microbiome, nematodes, mycorrhiza, protozoa, worms, etc.) through the trophic webs and different interactions between soil species, are going to regulate each other and the pathogens populations, avoiding disease outbreaks. In agroecosystems where plant diseases and epidemics are frequent and destructive, soil-borne plant pathogens has been managed applying different strategies: chemical, cultural, biological agents and others; however so far, there is not enough knowledge about how important is soil biodiversity, mainly microbiome diversity and soil food webs structure and function in the management of root pathogens, in root and plant health, in healthy food production, and maybe more relevant in the conservation of soil as a natural resource and derived from it, the ecosystem services important for life in our planet.

The enigma of Sir William Robert Wills Wilde (1815–1876)

William Wilde, father of Oscar Wilde, made a significant contribution to ophthalmology and otology. Qualified as a surgeon. educated in statistics and showing sympathy for the Irish population, Wilde was appointed a Commissioner for the 1851 Census, which covered the time of the Irish Famine (1845–1852). Wilde, steeped in Irish mythology, used his knowledge to develop a close rapport with the Irish peasantry. However, his life was a paradox; he supported the British Government's approach to the Famine and at the same time he showed humanity to the Irish peasantry. In his personal life he was implicated in an abortive libel case involving a young female patient who had accused him of rape. Wilde lived as though he had two separate lives : on the one hand the successful surgeon, famine Commissioner and cataloguer of Irish antiquities, and the other a countryman and disciple of Irish mythology. Wilde was highly preceptive especially in his views on the recording of medical data and outcomes in clinical practice. We argue that Wilde was probably unmatched in the variety of his talents but was also perplexing in the various actions he took during his life and that indeed Wilde was an enigma.

An oomycete effector subverts host vesicle trafficking to channel starvation-induced autophagy to the pathogen interface

Eukaryotic cells deploy autophagy to eliminate invading microbes. In turn, pathogens have evolved effector proteins to counteract antimicrobial autophagy. How adapted pathogens co-opt autophagy for their own benefit is poorly understood. The Irish famine pathogen Phytophthora infestans secretes the effector protein PexRD54 that selectively activates an unknown plant autophagy pathway that antagonizes antimicrobial autophagy at the pathogen interface. Here, we show that PexRD54 induces autophagosome formation by bridging vesicles decorated by the small GTPase Rab8a with autophagic compartments labeled by the core autophagy protein ATG8CL. Rab8a is required for pathogen-triggered and starvation-induced but not antimicrobial autophagy, revealing specific trafficking pathways underpin selective autophagy. By subverting Rab8a-mediated vesicle trafficking, PexRD54 utilizes lipid droplets to facilitate biogenesis of autophagosomes diverted to pathogen feeding sites. Altogether, we show that PexRD54 mimics starvation-induced autophagy to subvert endomembrane trafficking at the host-pathogen interface, revealing how effectors bridge distinct host compartments to expedite colonization.

Financial Inclusion with Hybrid Organizational Forms: Microfinance, Philanthropy, and the Poor Law in Ireland, c. 1836–1845

The turbulent 1830s saw a sequence of great political and social reforms in the United Kingdom. One such reform was the introduction of a locally funded Poor Law in Ireland. The development of a nascent welfare system in 1838 coincided with a boom in the formation of microfinance institutions in Ireland. The focus of this study is the expansion of a hybrid organizational form, Loan Fund Societies (LFSs), in the ten years prior to the Great Irish Famine of 1845–1849. LFSs were legally established with a conflictual structure: acting as commercially viable charitable institutions required to provide credit to the deserving poor (to enable them to be self-sufficient) while dedicating their “profits” to supporting the indigent poor. This study uses an analytical framework drawing inspiration from institutional logics to explore and better understand Irish microfinance in the early nineteenth century, a period of profound socioeconomic and socioreligious changes. It seeks to explain the factors that motivated the establishment and de-establishment of microfinance institutions amid this tumult. Legislative changes in LFS business parameters in 1843 made the tensions between being charitable and commercially sustainable salient; and, for some, it made continued existence untenable.

Global historic pandemics caused by the FAM-1 genotype of Phytophthora infestans on six continents

The FAM-1 genotype of Phytophthora infestans caused late blight in the 1840s in the US and Europe and was responsible for the Irish famine. We sampled 140 herbarium specimens collected between 1845 and 1991 from six continents and used 12-plex microsatellite genotyping (SSR) to identify FAM-1 and the mtDNA lineage (Herb-1/Ia) present in historic samples. FAM-1 was detected in approximately 73% of the historic specimens and was found on six continents. The US-1 genotype was found later than FAM-1 on all continents except Australia/Oceania and in only 27% of the samples. FAM-1 was the first genotype detected in almost all the former British colonies from which samples were available. The data from historic outbreak samples suggest the FAM-1 genotype was widespread, diverse, and spread to Asia and Africa from European sources. The famine lineage spread to six continents over 144 years, remained widespread and likely spread during global colonization from Europe. In contrast, modern lineages of P. infestans are rapidly displaced and sexual recombination occurs in some regions.