phytophthora infestans phytophthora infestans phytophthora infestans is an oomycete or water mold, a fungus-like microorganism that causes the serious potato and tomato disease known as late blight or potato blight. early blight, caused by alternaria solani, is also often called "potato blight". late blight was a major culprit in the 1840s european, the 1845–1852 irish, and the 1846 highland potato famines. the organism can also infect some other members of the solanaceae. the pathogen is favored by moist, cool environments: sporulation is optimal at 12–18 °c (54–64 °f) in water-saturated or nearly saturated environments, and zoospore production is favored at temperatures below 15 °c (59 °f). lesion growth rates are typically optimal at a slightly warmer temperature range of 20 to 24 °c (68 to 75 °f). phytophthora infestans symptom of late blight on the underside of a potato leaf scientific classification kingdom: chromista phylum: oomycota order: peronosporales family: peronosporaceae genus: phytophthora species: p. infestans binomial name phytophthora infestans(mont.) de bary etymology the genus name phytophthora comes from the greek φυτό–(phyto), meaning : "plant" – plus the greek φθορά (phthora), meaning : "decay, ruin, perish". the species name infestans is the present participle of the latin verb infestare, meaning : "attacking, destroying", from which we get the word "to infest". the name phytophthora infestans was coined in 1876 by the german mycologist heinrich anton de bary (1831–1888). life cycle, signs and symptoms infected potato life cycle on potato the asexual life cycle of phytophthora infestans is characterized by alternating phases of hyphal growth, sporulation, sporangia germination (either through zoospore release or direct germination, i.e. germ tube emergence from the sporangium), and the re-establishment of hyphal growth. there is also a sexual cycle, which occurs when isolates of opposite mating type (a1 and a2, see § mating types below) meet. hormonal communication triggers the formation of the sexual spores, called oospores. the different types of spores play major roles in the dissemination and survival of p. infestans. sporangia are spread by wind or water and enable the movement of p. infestans between different host plants. the zoospores released from sporangia are biflagellated and chemotactic, allowing further movement of p. infestans on water films found on leaves or soils. both sporangia and zoospores are short-lived, in contrast to oospores which can persist in a viable form for many years. people can observe phytophthora infestans produce dark green, then brown then black spots on the surface of potato leaves and stems, often near the tips or edges, where water or dew collects. the sporangia and sporangiophores appear white on the lower surface of the foliage. as for tuber blight, the white mycelium often shows on the tubers' surface. under ideal conditions, p. infestans completes its life cycle on potato or tomato foliage in about five days. sporangia develop on the leaves, spreading through the crop when temperatures are above 10 °c (50 °f) and humidity is over 75–80% for 2 days or more. rain can wash spores into the soil where they infect young tubers, and the spores can also travel long distances on the wind. the early stages of blight are easily missed. symptoms include the appearance of dark blotches on leaf tips and plant stems. white mold will appear under the leaves in humid conditions and the whole plant may quickly collapse. infected tubers develop grey or dark patches that are reddish brown beneath the skin, and quickly decay to a foul-smelling mush caused by the infestation of secondary soft bacterial rots. seemingly healthy tubers may rot later when in store. p. infestans survives poorly in nature apart from on its plant hosts. under most conditions, the hyphae and asexual sporangia can survive for only brief periods in plant debris or soil, and are generally killed off during frosts or very warm weather. the exceptions involve oospores, and hyphae present within tubers. the persistence of viable pathogen within tubers, such as those that are left in the ground after the previous year's harvest or left in cull piles is a major problem in disease management. in particular, volunteer plants sprouting from infected tubers are thought to be a major source of inoculum (or propagules) at the start of a growing season. this can have devastating effects by destroying entire crops. mating types the mating types are broadly divided into a1 and a2. until the 1980s populations could only be distinguished by virulence assays and mating types, but since then more detailed analysis has shown that mating type and genotype are substantially decoupled. these types each produce a mating hormone of their own. pathogen populations are grouped into clonal lineages of these mating types and includes: a1 a1 produces a mating hormone, a diterpene α1. clonal lineages of a1 include: cn-1cn-1, -2, -4, -5, -6, -7, -8 - mtdna haplotype ia, china in 1996-7 cn-3 - ia, china, 1996-7 cn-10 - ia, china, 2004 cn-11 - iib, china, 2000&2 cn01 - iia, china, 2004-9 cn03 - ia/iib, china, 2004-9 fam-1 - (only presumed to be a1), mtdna haplo ia subtype herb-1, japan, philippines, india, china, malaysia, nepal, present some time before 1950 in-1 - ia, india, nepal, 1993 in-2 - ia, india, 1993 jp-2jp-2/sib-1/rf006 - mtdna haplo iia, distinguishable by rg57, intermediate level of metalaxyl resistance, japan, china, korea, thailand, 1996–present jp-3 - iia, distinguishable by rg57, intermediate level of metalaxyl resistance, japan, 1996–present jp-4 - iia, distinguishable by rg57, intermediate level of metalaxyl resistance, japan, 1996–present kr-1 zhang sensu zhang (not to be confused with #kr-1 sensu gotoh below) - iia, korea, 2002-4 kr_1_a1kr_1_a1 - mtdna haplo unknown, korea, 2009-16 mo-6 - ia, china, 2004 np-1 - ia, india, nepal, 1993, 1996-7 np-2 - ia, nepal, 1997 np1 - ia, nepal, 1999-2000 np2 a1 - (also a2, see #the a2 type of np2 below) ia, nepal, 1999-2000 np3 (not to be confused with #us-1 below) - ib, nepal, 1999-2000 us-1 (not to be confused with #np3/us-1 above) - ib, china, india, nepal, japan, taiwan, thailand, vietnam, 1940-2000 np4, 5, 7, and 9 - ia, nepal, 1999-2000 np6 - mtdna haplo unknown, nepal, 1999-2000 us-11 - iib, taiwan, korea, vietnam, 1998-2016 us-16 - iib, china, 2002&4 us-17 - iia, korea, 2003-4 us-23 us-24 2_a1 - ia, indonesia, 2016-9 t30-4 a2 discovered by john niederhauser in the 1950s, in the toluca valley in central mexico, while working for the rockefeller foundation's mexican agriculture program. published in niederhauser 1956. a2 produces a mating hormone α2. clonal lineages of a2 include: cn02 - see #13_a2/cn02 below us-22 - with mtdna haplotype h-20 jp-1 - iia, japan, korea, indonesia, late 1980s-present kr-1 gotoh sensu gotoh (not to be confused with #kr-1 sensu zhang above) - iia, differs from jp-1 by one rg57 band, korea, 1992 kr_2_a2 - mtdna haplo unknown, korea, 2009-16 cn-9 - ia, china, 2001 np2 a2 - (also a1, see #the a1 type of np2 above) ia, nepal, 1999-2000 np8 - ib, nepal, 1999-2000 np10 & 11 - ia, nepal, 1999-2000 th-1 - ia, thailand, china, nepal, 1994&7 unknown - ib, india, 1996-2003 br-1 - brazil us-7 us-8 us-14 - iia, korea, 2002-3 13_a2/cn02 - ia, china, india, bangladesh, nepal, pakistan, myanmar, 2005-19 self-fertile a self-fertile type was present in china between 2009 and 2013. physiology piinf1 is the inf1 in p. infestans. hosts respond with autophagy upon detection of this elicitor, liu et al. 2005 finding this to be the only alternative to mass hypersensitivity leading to mass programmed cell death. genetics p. infestans is diploid, with about 8-10 chromosomes, and in 2009 scientists completed the sequencing of its genome. the genome was found to be considerably larger (240 mbp) than that of most other phytophthora species whose genomes have been sequenced; p. sojae has a 95 mbp genome and p. ramorum had a 65 mbp genome. about 18,000 genes were detected within the p. infestans genome. it also contained a diverse variety of transposons and many gene families encoding for effector proteins that are involved in causing pathogenicity. these proteins are split into two main groups depending on whether they are produced by the water mold in the symplast (inside plant cells) or in the apoplast (between plant cells). proteins produced in the symplast included rxlr proteins, which contain an arginine-x-leucine-arginine (where x can be any amino acid) sequence at the amino terminus of the protein. some rxlr proteins are avirulence proteins, meaning that they can be detected by the plant and lead to a hypersensitive response which restricts the growth of the pathogen. p. infestans was found to encode around 60% more of these proteins than most other phytophthora species. those found in the apoplast include hydrolytic enzymes such as proteases, lipases and glycosylases that act to degrade plant tissue, enzyme inhibitors to protect against host defence enzymes and necrotizing toxins. overall the genome was found to have an extremely high repeat content (around 74%) and to have an unusual gene distribution in that some areas contain many genes whereas others contain very few. the pathogen shows high allelic diversity in many isolates collected in europe. this may be due to widespread trisomy or polyploidy in those populations.: 61 research study of p. infestans presents sampling difficulties in the united states.: 43 it occurs only sporadically and usually has significant founder effects due to each epidemic starting from introduction of a single genotype.: 43 origin and diversity of p. infestans histological model of a potato leaf cross-section, botanical museum greifswald the highlands of central mexico are considered by many to be the center of origin of p. infestans, although others have proposed its origin to be in the andes, which is also the origin of potatoes. a recent study evaluated these two alternate hypotheses and found conclusive support for central mexico being the center of origin. support for mexico – specifically the toluca valley – comes from multiple observations including the fact that populations are genetically most diverse in mexico, late blight is observed in native tuber-bearing solanum species, populations of the pathogen are in hardy–weinberg equilibrium, the two mating (see § mating types above) types occur in a 1:1 ratio, and detailed phylogeographic and evolutionary studies. furthermore, the closest relatives of p. infestans, namely p. mirabilis and p. ipomoeae are endemic to central mexico. on the other hand, the only close relative found in south america, namely p. andina, is a hybrid that does not share a single common ancestor with p. infestans. finally, populations of p. infestans in south america lack genetic diversity and are clonal. migrations from mexico to north america or europe have occurred several times throughout history, probably linked to the movement of tubers. until the 1970s, the a2 mating type was restricted to mexico, but now in many regions of the world both a1 and a2 isolates can be found in the same region. the co-occurrence of the two mating types is significant due to the possibility of sexual recombination and formation of oospores, which can survive the winter. only in mexico and scandinavia, however, is oospore formation thought to play a role in overwintering. in other parts of europe, increasing genetic diversity has been observed as a consequence of sexual reproduction. this is notable since different forms of p. infestans vary in their aggressiveness on potato or tomato, in sporulation rate, and sensitivity to fungicides. variation in such traits also occurs in north america, however importation of new genotypes from mexico appears to be the predominant cause of genetic diversity, as opposed to sexual recombination within potato or tomato fields. in 1976 - due to a summer drought in europe - there was a potato production shortfall and so eating potatoes were imported to fill the shortfall. it is thought that this was the vehicle for mating type a2 to reach the rest of the world. in any case, there had been little diversity, consisting of the us-1 strain, and of that only one type of: mating type, mtdna, restriction fragment length polymorphism, and di-locus isozyme. then in 1980 suddenly greater diversity and a2 appeared in europe. in 1981 it was found in the netherlands, united kingdom, 1985 in sweden, the early 1990s in norway and finland, 1996 in denmark, and 1999 in iceland. in the uk new a1 lineages only replaced the old lineage by end of the '80s, and