Mātauranga Māori and anti-microbials: Searching for new tools to control the spread of Kauri Dieback

<p>Phytophthora are plant pathogens, well known for devastating thousands of ecologically, culturally and economically significant plant crops worldwide. In greek Phytophthora translates directly to ‘plant destroyer’. Though it is ‘fungus-like’, Phytophthora are eukaryotic oomycetes, more closely related to brown algae and diatoms. Phytophthora have three key lifecycle stages: oospores, zoospores, and mycelia. Kauri are ancient conifer species dating back to the Cretaceous period (145 mya) and are now rapidly declining due to Kauri dieback caused by Phytophthora agathidicida. P.agathadicida causes root rot in Kauri trees and was first misidentified as P. hevave on Great Barrier Island in the early 1970s. Its origin is unknown however research argues it may have evolved from P. infestans, the pathogen that caused the Irish potato famine in 1845. For Te Āo Māori, Kauri are highly regarded tīpuna (ancestors) and Kauri Dieback is alarming to many Northern Iwi. Kauri wood and resin are highly sought and economically valuable resources. The Waipoua forest is the largest Kauri forest and the most impacted by Kauri Dieback. Over 25% of Kauri in the Waitākere ranges are either infected with P. agathadicida or are symptomatic, a percentage that is steadily increasing. A rāhui (temporary ban) was placed on the Waitākere ranges by local iwi Te Kawerau a Maki in 2018 as a preventative measure to reduce movement of P. agathadicida in soil. Apart from track closures, scrubbing and spraying equipment - before and after entering the forest - is the only tool of management. Sterigene disinfectant is the only treatment to reduce the spread of Kauri Dieback. Sterigene kills zoospores, mycelia and sporangium but is ineffective against P. agathidicida oospoores. Sexually produced oospores are responsible for the long-term survival of Phytophthora as they have a thick cell wall. The first part of this thesis examines a range of commercially available disinfectants and their efficacy against P. agathidicida oospores. These results confirm that Sterigene and/or Trigene are not effective against P. agathidicida oospores. My results also show that 2% bleach, 1% Virkon, and 70% ethanol all reduce oospore viability. Napisan also reduced oospore viability, but also interacted with the viability stains, therefore further investigations are needed. Napisan is an oxygen bleach, commercially affordable and easily accessible in supermarkets. Unlike sterigene and bleach, Napisan is safe to use on clothes, wool and soft textiles. If effective against oospores and the other lifecycle stages, Napisan could be a promising solution to help reduce the spread of Kauri Dieback.</p>

Mātauranga Māori and anti-microbials: Searching for new tools to control the spread of Kauri Dieback

<p>Phytophthora are plant pathogens, well known for devastating thousands of ecologically, culturally and economically significant plant crops worldwide. In greek Phytophthora translates directly to ‘plant destroyer’. Though it is ‘fungus-like’, Phytophthora are eukaryotic oomycetes, more closely related to brown algae and diatoms. Phytophthora have three key lifecycle stages: oospores, zoospores, and mycelia. Kauri are ancient conifer species dating back to the Cretaceous period (145 mya) and are now rapidly declining due to Kauri dieback caused by Phytophthora agathidicida. P.agathadicida causes root rot in Kauri trees and was first misidentified as P. hevave on Great Barrier Island in the early 1970s. Its origin is unknown however research argues it may have evolved from P. infestans, the pathogen that caused the Irish potato famine in 1845. For Te Āo Māori, Kauri are highly regarded tīpuna (ancestors) and Kauri Dieback is alarming to many Northern Iwi. Kauri wood and resin are highly sought and economically valuable resources. The Waipoua forest is the largest Kauri forest and the most impacted by Kauri Dieback. Over 25% of Kauri in the Waitākere ranges are either infected with P. agathadicida or are symptomatic, a percentage that is steadily increasing. A rāhui (temporary ban) was placed on the Waitākere ranges by local iwi Te Kawerau a Maki in 2018 as a preventative measure to reduce movement of P. agathadicida in soil. Apart from track closures, scrubbing and spraying equipment - before and after entering the forest - is the only tool of management. Sterigene disinfectant is the only treatment to reduce the spread of Kauri Dieback. Sterigene kills zoospores, mycelia and sporangium but is ineffective against P. agathidicida oospoores. Sexually produced oospores are responsible for the long-term survival of Phytophthora as they have a thick cell wall. The first part of this thesis examines a range of commercially available disinfectants and their efficacy against P. agathidicida oospores. These results confirm that Sterigene and/or Trigene are not effective against P. agathidicida oospores. My results also show that 2% bleach, 1% Virkon, and 70% ethanol all reduce oospore viability. Napisan also reduced oospore viability, but also interacted with the viability stains, therefore further investigations are needed. Napisan is an oxygen bleach, commercially affordable and easily accessible in supermarkets. Unlike sterigene and bleach, Napisan is safe to use on clothes, wool and soft textiles. If effective against oospores and the other lifecycle stages, Napisan could be a promising solution to help reduce the spread of Kauri Dieback.</p>

PROGRESSES ON THE NATURE AND BIOTIC STRESS OF POTATO (SOLANUM TUBEROSUM L.)

Potato (Solanum tuberosum L.) is the third largest crop in terms of consumption by human, most important tuber crop in the world and a vital plant for global food security. Instead, potato breeding is slow compared to other crops. Transforming potato into a diploid F1 hybrid crop is a hopeful method to increase potato genetic gain. Studies on breeding and genetics of potato has big potential to solve many problems exist in potato. Another potential area for these studies are diseases which are seriously targeting this crop worlwide started from Irish potato famine which effected whole Europe continent. Here in this review, some of latest significant problems and approaches related to potato production are given below.

Regressive evolution of an effector following a host jump in the Irish Potato Famine Pathogen Lineage

In order to infect a new host species, the pathogen must evolve to enhance infection and transmission in the novel environment. Although we often think of evolution as a process of accumulation, it is also a process of loss. Here, we document an example of regressive evolution in the Irish potato famine pathogen (Phytophthora infestans) lineage, providing evidence that a key sequence motif in the effector PexRD54 has degenerated following a host jump. We began by looking at PexRD54 and PexRD54-like sequences from across Phytophthora species. We found that PexRD54 emerged in the common ancestor of Phytophthora clade 1b and 1c species, and further sequence analysis showed that a key functional motif, the C-terminal ATG8-interacting motif (AIM), was also acquired at this point in the lineage. A closer analysis showed that the P. mirabilis PexRD54 (PmPexRD54) AIM appeared unusual, the otherwise-conserved central residue mutated from a glutamate to a lysine. We aimed to determine whether this PmPexRD54 AIM polymorphism represented an adaptation to the Mirabilis jalapa host environment. We began by characterizing the M. jalapa ATG8 family, finding that they have a unique evolutionary history compared to previously characterized ATG8s. Then, using co-immunoprecipitation and isothermal titration calorimetry assays, we showed that both full-length PmPexRD54 and the PmPexRD54 AIM peptide bind very weakly to the M. jalapa ATG8s. Through a combination of binding assays and structural modelling, we showed that the identity of the residue at the position of the PmPexRD54 AIM polymorphism can underpin high-affinity binding to plant ATG8s. Finally, we conclude that the functionality of the PexRD54 AIM was lost in the P. mirabilis lineage, perhaps owing to as-yet-unknown pressure on this effector in the new host environment.Author SummaryPathogens evolve in concert with their hosts. When a pathogen begins to infect a new host species, known as a “host jump,” the pathogen must evolve to enhance infection and transmission. These evolutionary processes can involve both the gain and loss of genes, as well as dynamic changes in protein function. Here, we describe an example of a pathogen protein that lost a key functional domain following a host jump, a salient example of “regressive evolution.” Specifically, we show that an effector protein from the plant pathogen Phytopthora mirabilis, a host-specific lineage closely related to the Irish potato famine pathogen Phytopthora infestans, has a derived amino acid polymorphism that results in a loss of interaction with certain host machinery.

Dynamic localization of a helper NLR at the plant–pathogen interface underpins pathogen recognition

Plants employ sensor–helper pairs of NLR immune receptors to recognize pathogen effectors and activate immune responses. Yet, the subcellular localization of NLRs pre- and postactivation during pathogen infection remains poorly understood. Here, we show that NRC4, from the “NRC” solanaceous helper NLR family, undergoes dynamic changes in subcellular localization by shuttling to and from the plant–pathogen haustorium interface established during infection by the Irish potato famine pathogen Phytophthora infestans. Specifically, prior to activation, NRC4 accumulates at the extrahaustorial membrane (EHM), presumably to mediate response to perihaustorial effectors that are recognized by NRC4-dependent sensor NLRs. However, not all NLRs accumulate at the EHM, as the closely related helper NRC2 and the distantly related ZAR1 did not accumulate at the EHM. NRC4 required an intact N-terminal coiled-coil domain to accumulate at the EHM, whereas the functionally conserved MADA motif implicated in cell death activation and membrane insertion was dispensable for this process. Strikingly, a constitutively autoactive NRC4 mutant did not accumulate at the EHM and showed punctate distribution that mainly associated with the plasma membrane, suggesting that postactivation, NRC4 may undergo a conformation switch to form clusters that do not preferentially associate with the EHM. When NRC4 is activated by a sensor NLR during infection, however, NRC4 forms puncta mainly at the EHM and, to a lesser extent, at the plasma membrane. We conclude that following activation at the EHM, NRC4 may spread to other cellular membranes from its primary site of activation to trigger immune responses.

Dynamic accumulation of a helper NLR at the plant-pathogen interface underpins pathogen recognition

Plants employ sensor-helper pairs of NLR immune receptors to recognize pathogen effectors and activate immune responses. Yet the subcellular localization of NLRs pre- and post- activation during pathogen infection remains poorly known. Here we show that NRC4, from the 'NRC' solanaceous helper NLR family, undergoes dynamic changes in subcellular localization by shuttling to and from the plant-pathogen haustorium interface established during infection by the Irish potato famine pathogen Phytophthora infestans. Specifically, prior to activation, NRC4 accumulates at the extra-haustorial membrane (EHM), presumably to mediate response to perihaustorial effectors, that are recognized by NRC4-dependent sensor NLRs. However not all NLRs accumulate at the EHM, as the closely related helper NRC2, and the distantly related ZAR1, did not accumulate at the EHM. NRC4 required an intact N- terminal coiled coil domain to accumulate at the EHM, whereas the functionally conserved MADA motif implicated in cell death activation and membrane insertion was dispensable for this process. Strikingly, a constitutively autoactive NRC4 mutant did not accumulate at the EHM and showed punctate distribution that mainly associated with the plasma membrane, suggesting that post-activation, NRC4 probably undergoes a conformation switch to form clusters that do not preferentially associate with the EHM. When NRC4 is activated by a sensor NLR during infection however, NRC4 formed puncta mainly at the EHM and to a lesser extent at the plasma membrane. We conclude that following activation at the EHM, NRC4 may spread to other cellular membranes from its primary site of activation to trigger immune responses.

Singing and dancing in the cruellest month: A reflection on theology and poetry in a time of COVID

This article explores what contribution poetry and the arts can make to the human experience in a time of pandemic. It argues that artistic productions can ‘enlarge the heart’ such that sorrow and anxiety are not removed or defeated but are, as in the biblical text, ‘woven […] into a larger imaginative story.’ This argument is made through close examination of three poems: T. S. Eliot’s “The Waste Land”, written in 1922 during the Spanish flu epidemic; “Quarantine” by Eavan Boland, set during the Irish Potato Famine of the 1840s; and Malcolm Guite’s “Easter 2020”.

Recreation of the Edinburgh Potato Solanum ×Edinense Berthault

Solanum ×edinense Berthault, is a spontaneously occurring hybrid between S. demissum Lindl. and the cultivated potato, S. tuberosum L., found near potato fields in Mexico. Although not described until 1911, this hybrid was in cultivation at the Royal Botanic Garden Edinburgh shortly after the Irish Potato Famine of 1845–1849 and proved to be highly resistant to late blight, Phytophthora infestans. In the mid-19th century late blight caused widespread failure of the potato crop across Europe and played a central role in the Irish Potato Famine. Using the parent species in controlled crosses we have recreated the hybrid that was named by Berthault in recognition of the Royal Botanic Garden Edinburgh as the source of his plant material. We have also researched the early history of this hybrid potato in Edinburgh and demonstrated disease resistance through field exposure during the outbreak of late blight in Edinburgh in 2019. This work underlines the important role of this hybrid in the breeding of disease resistant potato cultivars.

Genome-Wide Increased Copy Number is Associated with Emergence of Dominant Clones of the Irish Potato Famine Pathogen Phytophthora infestans

ABSTRACT The plant pathogen that caused the Irish potato famine, Phytophthora infestans, continues to reemerge globally. These modern epidemics are caused by clonally reproducing lineages. In contrast, a sexual mode of reproduction is observed at its center of origin in Mexico. We conducted a comparative genomic analysis of 47 high-coverage genomes to infer changes in genic copy number. We included samples from sexual populations at the center of origin as well as several dominant clonal lineages sampled worldwide. We conclude that sexual populations at the center of origin are diploid, as was the lineage that caused the famine, while modern clonal lineages showed increased copy number (3×). Copy number variation (CNV) was found genome-wide and did not to adhere to the two-speed genome hypothesis. Although previously reported, tetraploidy was not found in any of the genomes evaluated. We propose a model of dominant clone emergence supported by the epidemiological record (e.g., EU_13_A2, US-11, US-23) whereby a higher copy number provides fitness, leading to replacement of prior clonal lineages. IMPORTANCE The plant pathogen implicated in the Irish potato famine, Phytophthora infestans, continues to reemerge globally. Understanding changes in the genome during emergence can provide insights useful for managing this pathogen. Previous work has relied on studying individuals from the United States, South America, Europe, and China reporting that these can occur as diploids, triploids, or tetraploids and are clonal. We studied variation in sexual populations at the pathogen’s center of origin, in Mexico, where it has been reported to reproduce sexually as well as within clonally reproducing, dominant clones from the United States and Europe. Our results newly show that sexual populations at the center of origin are diploid, whereas populations elsewhere are more variable and show genome-wide variation in gene copy number. We propose a model of evolution whereby new pathogen clones emerge predominantly by increasing the gene copy number genome-wide.