David entered the field of genetics in one of its glorious decades. Beadle and Tatum had begun a revolutionary program in 1941 with their discovery of mutations in Neurospora that blocked biosynthetic reactions (BEADLE and TATUM 1941). Francis Ryan, David's Ph.D. mentor, was an early postdoctoral associate of the Beadle–Tatum laboratory at Stanford in 1941 and returned to his home base at Columbia University, dedicated to the study of microbial and biochemical genetics. After World War II, David joined Ryan as one of the first generation of students in the new era. David, inspired by Neurospora tetrad analysis, chose the corn pathogen, Ustilago maydis, for his thesis work, but switched to Neurospora thereafter, doubtless recognizing its methodological advantages and the increasing visibility of Neurospora research. David eschewed direct involvement in biochemical work and instead embarked upon detailed studies on the genetics of Neurospora, which he continued for the rest of his career. This put him in a unique position as a pioneer in the genetics of haploid eukaryotes and as the facilitator of research by all later investigators who used Neurospora as an experimental organism. As Charley Yanofsky said in a recent memorial, "Beadle and Tatum initiated research using this organism, but it was David who made certain that this interest would continue."

The sexual phase of Neurospora was discovered by B. O. Dodge (SHEAR and DODGE 1927). An arresting feature of the eight-spored species, N. crassa and N. sitophila, was the alignment of meiotic products (each duplicated in a postmeiotic division) in the linear tetrad, or ascus. The products of the first-division segregation remain in the upper and lower halves, and the second-division segregation products remain adjacent. Dodge discovered not only that alleles of a single gene (the mating type A/a, in his case) segregated 4A: 4a, but also that some asci displayed a 2A:2a:2A:2a pattern. The latter was interpreted by Beadle, among others, as a result of second-division segregation, showing clearly that crossing over occurred at the four-strand stage of meiosis. Analysis of tetrads displayed the highly deterministic nature of meiosis more clearly than earlier analyses. Nevertheless, the technical ease of dissecting products (ascospores) of a single meiosis, together with the increasing availability of biochemical markers, popularized Neurospora for genetic investigations. With the further investigations and development of standard strains by Carl Lindegren in the 1930s and the Beadle laboratory in the 1940s, tetrad analysis came into its own, and David became one of its greatest practitioners.

Formal genetic work and the formation of the Neurospora community:

David's early work on N. crassa focused on linkage analysis using tetrads and random progeny to study mapping functions and interference and to construct dependable genetic maps. The methods were especially useful for species with unordered tetrads. He could now use many new mutants isolated in his own and other laboratories, especially Beadle's, which had by then moved to the California Institute of Technology. At this time, he and Dot had teamed up with Raymond Barratt, another Tatum student, to publish the first "compendium" of Neurospora mutants in 1954 (BARRATT et al. 1954). This was less a curatorial job than the first bible of Neurospora genetic theory and techniques. The long work included not only theoretical analysis of recombination, but also phenotypic descriptions of all known mutants and their alleles and maps of Neurospora's seven chromosomes. Barratt had already proposed the main nomenclatural and certain other conventions of the field. Their joint work led Barratt, at Dartmouth after 1954, to establish the Fungal Genetics Stock Center, to organize the first Neurospora Information Conference (now the Fungal Genetics Conference), and to publish the Neurospora Newsletter (now the Fungal Genetics Newsletter). These achievements established and bound together a Neurospora research community that has endured to this day. David, while still collaborating with Barratt in the curatorial work, continued his steady output of original work. He would soon become the central player in keeping the Neurospora community together and in defining Neurospora as a model organism for many areas of research. Part of the success of this effort reflects David's instilling a lack of competitiveness into the field as a whole; he shared and trusted, expecting the same from others. (A paragon of fairness, he never put his name on articles from his lab unless he had done some of the experimental work.)

Chromosomal aberrations and cytogenetics:

In the early 1960s, David focused on chromosomal aberrations. X-ray and ultraviolet mutagenesis, the latter commonly used by Neurospora workers, yield chromosomal rearrangements, some associated with mutations at the breakpoints. David's linkage studies uncovered these aberrations, which he interpreted straightforwardly as chiefly reciprocal or insertional translocations. Such rearrangements led to characteristic patterns of ascospore abortion in tetrads. David developed his observations into a methodology of detecting and characterizing genetic aberrations in ways the rest of the community could use routinely for creating duplications, deficiencies, and fine-scale mapping of closely linked mutants by duplication coverage.

One of the most useful tools emerging from this work was a multiply translocated strain called alcoy, in which interchanges had occurred among six of Neurospora's seven chromosomes (PERKINS et al. 1969). The strain also carried the "visible" mutations al-1, cot, and ylo (albino, colonial temperature sensitive, and yellow, respectively). Because translocations restrict recombinant survival, the chromosome assignment of a new mutation could be inferred by visual inspection of progeny in as little as a single cross. Follow-up crosses could quickly lead to the assignment of the map position of the alteration in the new mutant. This enabled even biochemists unfamiliar with genetics (or, more commonly, their students unfamiliar with genetics) to map new mutations and to submit the information to the Fungal Genetics Stock Center. Through contributions like alcoy and a variety of efficient genetic and microbiological techniques, David's laboratory took its place as an international intellectual resource. His laboratory underlay the growing fusion of genetics with biochemistry and, eventually, with molecular biology, in Neurospora research.

The major outcome of the work on chromosomal aberrations in David's own laboratory was the development of Neurospora cytogenetics, at first in collaboration with his student, Edward Barry (PERKINS and BARRY 1977; PERKINS 1997). McClintock and Singleton had shown that the cytology of meiosis in Neurospora was orthodox (MCCLINTOCK 1945; SINGLETON 1953), and David showed that chromosomal aberrations behaved as they did in corn. But the cytogenetic work soon became a window on novel phenomena of considerable interest, some of which continue to surprise current researchers. Most duplications, arising in crosses of translocations with normal-sequence strains, are viable (although mostly infertile with the standard strain). These provided material for the study of gene dosage and the relation of alleles in a single nucleus vs. their relation in heterokaryotic mycelia (where alleles are located in different nuclei). It also provided, through duplications arising in standard X translocation crosses, the means for detecting and analyzing the variety of vegetative incompatibility genes in nature: heterozygotes for such genes (arising as duplications in meiosis) are likely to be seriously debilitated as the result of incompatibility reactions (MYLYK 1975). More recently, David showed that nonhomologous (ectopic) integration of transforming DNA is often associated with chromosomal aberrations. The sterility of many duplication strains can now be attributed in many cases to extensive repeat-induced point mutation (RIP) in the premeiotic stage of the ascus (SELKER 1999) or to meiotic silencing of unpaired DNA during meiosis itself (SHIU et al. 2001). The extraordinary collection of aberrant strains has gone from what many might have considered an exotic hobby to a major tool in the study of genome dynamics in this simple organism.

In 1974, Namboori Raju ("Raju") joined the Perkins laboratory and extended its work in important ways. For >32 years, Raju worked closely with David, taking advantage of a variety of mutants affecting meiotic development in Neurospora. The cytological insight emerging from this work is without parallel in the fungi (RAJU 1992). This side of the laboratory's effort has contributed to the remarkable molecular biological knowledge of meiosis, covering nuclear interactions, spore delimitation, gene expression in the meiotic stages (through the use of green fluorescent protein), and meiotic silencing. The work has illuminated in retrospect much of the previous work in the laboratory about the formal genetics of aberrant chromosomes, the behavior of duplications and deficiencies in meiosis, and the many mutant loci affecting ascus development (many initially isolated by Dot).

Genetics of natural populations:

Eighty-four years separated the description of the asexual and the sexual phases of Neurospora. As indicated above, mating is governed by the mating-type locus, with two alleles. Both strains can mate as males (in the lab, via asexual spores, or macroconidia) or females (via protoperithecia, the unfertilized sexual structure). Yet, only strains of opposite mating type can cross, rendering Neurospora an outbred species. Perithecia, the fertilized female structures in which the meiotic cells develop, rarely become visible in nature. However, Neurospora colonies appear rapidly after fires in forested areas or areas with burned vegetation, revealing themselves with their abundant tufts of orange macroconidia. This is consistent with the knowledge that, in the laboratory, ascospore germination requires heat activation, a technique used in the laboratory since the time of Dodge. David began to pursue the biology of natural Neurospora populations with simple questions: Was Neurospora a clonal species, propagating locally by means of macroconidia? What are the means of dispersal of Neurospora propagules? Is the mating pool global, regional, or highly parochial? What is the genetic heterogeneity in local and global populations? These matters had rarely been investigated in haploid eukaryotes, and David recognized Neurospora as extremely favorable material for such studies.

After some difficulty with collections of airborne spores, David decided to sample Neurospora spp. all over the world, both by travel and by asking trusted collaborators to make collections in their areas. He rarely went abroad without a large supply of collection envelopes. He visited exotic locations spanning the globe from Indonesia, Africa, South America, and much of the rest of the habitable world (and, as Ambrose Bierce would say, Canada). His letters home about his adventures rival his scientific findings in interest.

Barbara Turner joined the laboratory in the 1960s. She was mainly responsible for processing the collected material, beginning with David's first collecting trip in 1968. She developed testers for species assignments, purified strains, maintained the expanding records, and worked independently on novel findings (PERKINS et al. 1976; PERKINS and TURNER 1988). By the time of the last publication on wild-collected strains (TURNER et al. 2001), a massive amount of work had been done with the strains by the Perkins laboratory and many others around the world. As David concluded early on, "The collections are a source of variants in structural and regulatory genes, of genes governing vegetative incompatibility, and of information on genetic variability within and between populations" (PERKINS et al. 1976, p. 310).

The findings arising from the wild collections surprised most of us. First, using multiple samples from single areas, the laboratory established that >75% of new colonies were homokaryotic and that the mating types of colonies were approximately equal in frequency. Later it was found that heterokaryon compatibility alleles (which restrict mycelial fusion) were quite diverse among samples (MYLYK 1976) and that allozyme variation in one site was comparable to the variation among all the sites sampled in a broader area (SPIETH 1975). Second, crosses of samples from widely separated areas were usually fertile, rendering fertility with authentic testers the most practical indicator of species (PERKINS 1994). In fact, a new species, N. discreta, was identified during the course of such tests (PERKINS and RAJU 1986).

The conclusions from this work were that ascospores initiate most Neurospora growth following fires and that, although conidia are produced in abundance, they are not viable for long and may not account for long-range dispersal. They could, however, account for local dispersal in unburned substrates such as bakeries, sugar cane processing plants, and the like. An interesting, detailed study of this matter has been published by PANDIT and MAHESHWARI (1996). David Jacobson, a more recent senior associate in the laboratory, has promoted more extensive studies of Neurospora in nature. Studies emerging from this work have given more texture to the picture of variation and dispersal of Neurospora spp. It may be that these plants may have to die (by fire or other means) before they become substrates for profligate growth of Neurospora; ascospores may be activated more often in nature by chemicals (e.g., furfural) released by decaying plants than by heat; and the identity of propagules that initiate infections remains unclear (POWELL et al. 2003), especially in view of the very few reports of finding perithecia in nature.

A remarkable novel factor turned up early in the study of the wild-collected strains. TURNER and PERKINS (1979) detected strains of N. sitophila and N. intermedia carrying chromosomal meiotic drive elements named Spore killer (Sk-1, -2, and -3). In individual asci, these elements kill sibling ascospores that do not carry them, leading to segregation distortion similar to meiotic drive elements in Drosophila, but more accessible to experimental work. Studies on the geographic distribution, heterogeneity, cytology, and suppression of meiotic gene silencing by Sk elements have preoccupied the laboratory for >30 years (TURNER 2001; RAJU 2002).

David, with his enormous body of work on genetics, cytogenetics, and population biology, remained in close contact with Neurospora workers around the world, both at meetings and in reciprocal visits between laboratories. He was a superb listener. Participants at the official meetings of Neurospora workers and fungal geneticists at the Asilomar Conference Center near Stanford would extend their stays by visiting his laboratory. His interests were broad, his memory phenomenal. Years after a visit, he would send a short note or card to the visitor, bringing to his or her attention an item or idea that might be helpful. Such attention from David was more than flattering to investigators; it inspired new experiments and bound them more closely to the community.

The genomic era:

David's continuing attention to his resources for the Neurospora community led him to take part in the advent of molecular work on the organism, beginning in the 1980s. His laboratory was a source of particular strains and other genetic tools for molecular biologists. At this time, Charley Yanofsky, after many years of work on bacteria, returned to Neurospora research at the instigation of his student, Erik Selker. Charley's laboratory was across the hall from the Perkins laboratory. Together, David and Charley fostered a new generation of research on Neurospora by a sophisticated group of graduate students and postdoctoral associates. The informal collaboration and social interactions of the two laboratories speeded the pace of discovery and placed Neurospora in the forefront of molecular research on fungi.

By the mid-1980s, molecular approaches to all fungi were the norm, and, now sharing a common language, the field of fungal genetics and biology was born (DAVIS and PERKINS 2002). Workers on all species of filamentous fungi recognized the importance and the uses of the model organism that Neurospora had become for this group of organisms. David's genetic work greatly facilitated the sequencing of the N. crassa genome, complete by 2000 (see GALAGAN et al. 2003). It was a great satisfaction to him and the field that the last major compendium of Neurospora mutants and maps, published in 2001 (PERKINS et al. 2001), could incorporate the molecular findings of many genes. The molecular research on Neurospora to which the Perkins laboratory contributed include studies of mating type, the RIP process, biological clocks, vegetative and meiotic gene silencing, evolutionary studies of individual systems (the mating-type chromosome especially), the genome sequence of N. crassa, and the origin and differences among Neurospora spp., especially by molecular phylogenetic means (e.g., SKUPSKI et al. 1997; DETTMAN et al. 2003). Thus the Perkins laboratory became a virtual continent on which Neurospora studies have evolved, and on which the rest of fungal genetics received its bearings and began to diversify in its own new ways.

David took pride that he was funded by the National Institutes of Health (NIH) continuously for a record 42 years and by the National Science Foundation for all his years of research thereafter. He received an NIH Research Career Award (1964–1989) and an NIH MERIT Award (1987–1996).

David was a citizen of science. In the world of genetics, he contributed his scientific findings in a modest, but very public way. He assumed the job of editor-in-chief of GENETICS (1963–1967), reviving the journal from a period of decline in quality and timely publication. He became president of the Genetics Society of America in 1977. He was elected to the National Academy of Sciences in 1981, was named a Guggenheim Fellow from 1983 to 1985, and was awarded the Genetics Society of America Morgan Medal in 1994. The British Mycological Society made him an Honorary Member in 2005.

As I indicated at the beginning of this article, Dot was understandably unsure of a future in science. She took a tortuous path from pharmacy, to the biomedical industry, to a role as a lab technician, and finally to her Ph.D. work with Tatum. Unlike David, her original interests lay in biochemical genetics, developing rapidly in Tatum's laboratory with her thesis and first publication on tryptophan mutants of Neurospora (NEWMEYER and TATUM 1953). Once she became part of David's life and lab, she contributed greatly to the formal genetics of Neurospora, making many independent contributions. However, she continued with biochemical genetics with her definitive genetic studies of the last steps of arginine metabolism (NEWMEYER 1962), work that crucially complemented my own later studies.

Her involvement with David's genetic studies deepened with time, yet her publications reflect the independence with which she worked. She sought increasingly to tie up loose ends. She pursued issues meticulously, extending the formal genetics of unassigned mutants, describing the effect of duplications, and refining the phenotypic description of problematic strains. It is a tribute to both David and Dot that David did not co-author publications that were truly her work, nor did either one hesitate to co-author articles on which they clearly collaborated. Others recall in a memorial tribute (http://www.stanford.edu/group/neurospora/index.html) that it was she who did the final editing of David's articles, making sure that his or their arguments were clearly tied to the data. Indeed, as I and many others attest, her interests remained extremely broad. In conversation, she absorbed a great deal and could point to missing elements in almost any scientific argument that her friends might make. She did so with a relentless logic and an equally relentless decency that inspired those with whom she spoke.

Her intellectual strength, combined with equal devotion to David and to good science, made her a fit collaborator and companion for the 54 years of their marriage. Unhappily, her health began to fail in the 1970s and she therefore had less to give to the laboratory as time went on. Nevertheless, she remained engaged with scientific interests, political activity, music, and literature until late in life. Through her life, we can appreciate how far we have come in bringing women to biology (if not to the other sciences). She was a woman in the science of her time, working with enthusiasm and responsibility in an environment illuminated by an equally gracious and generous husband.

Dot and David shared personality traits and interests. They will be remembered by friends well after their laboratory's contributions become "nameless"—that is, so embedded in the field that the discoverers are no longer cited. Both of them grew up in strong families that became impoverished during the Great Depression. They learned the values of hard work, frugality, education, cooperation, and generosity. These traits were strengthened as they worked their ways through college and graduate school. They were generous to visitors, carried on continuous correspondence with friends and colleagues, and collaborated with no sense of ownership of a research program. They were both knowledgeable and interested in research far from their own activities, allowing David to speak and write about them lucidly. They nurtured the careers of those new to the field, especially the young, and set an example of personal and scientific integrity for the field.

Charley Yanofsky always found David at work on weekends, and he endured interruptions with grace and attention. He bicycled to work to arrive 6 o'clock in the morning, used the stairs instead of the elevator, and even in his 80s, lay on the floor under his desk in the lab to get regular rest around noon. Dot was an ardent peace activist, and despite her shyness and poor health, she did as much as she could to petition the government to refrain from war. She drew David into this effort despite his own preoccupation with the laboratory. Both of them lived their sense of social responsibility, with a modest house and simple personal habits. Both insisted on integrity in political argument and reacted strongly and clearly to mendacities of the governing elite.

According to Susan Perkins, David spent increasing amounts of time and energy in his last years taking care of household affairs and of Dot as her health worsened. He hired day-time help for Dot and mostly managed to get to the lab 5 or 6 days a week. Generous to the end, he spent much of his time facilitating the work of other researchers and assuring the continuation of Neurospora's role as a model experimental organism by contributing to the online Neurospora Methods Protocols (http://www.fgsc.net/neurospora/neurospora.html). He could devote little time to his own experiments, but some months before his death he celebrated submitting the final version of an article to GENETICS, work that Dot pronounced "a masterpiece" (PERKINS et al. 2007).

As shining examples of openness, diligence, breadth of interest, and robust conscience, they leave us grateful for the riches they bestowed on the world of science and their global community of friends.

I deeply thank David Jacobson, Barbara Turner, Charles Yanofsky, Robert Metzenberg, Namboori Raju, and Susan Perkins for their clarifications, corrections, and contributions to this article.

BARRATT, R. W., D. NEWMEYER, D. D. PERKINS and L. GARNJOBST, 1954 Map construction in Neurospora crassa. Adv. Genet. 6: 1–93.[Medline]

BEADLE, G. W., and E. L. TATUM, 1941 Genetic control of biochemical reactions in Neurospora. Proc. Natl. Acad. Sci. USA 27: 499–506.[Free Full Text]

DAVIS, R. H., 2000 Neurospora: Contributions of a Model Organism. Oxford University Press, New York.

DAVIS, R. H., and D. D. PERKINS, 2002 Neurospora: a model of model microbes. Nat. Rev. Genet. 3: 397–403.[Medline]

DETTMAN, J. R., D. J. JACOBSON, E. TURNER, A. PRINGLE and J. W. TAYLOR, 2003 Reproductive isolation and phylogenetic divergence in Neurospora: comparing methods of species recognition in a model eukaryote. Evolution 57: 2721–2741.[CrossRef][Medline]

GALAGAN, J. E., S. E. CALVO, K. A. BORKOVICH, E. U. SELKER, N. D. READ et al., 2003 The genome sequence of the filamentous fungus Neurospora crassa. Nature 422: 859–868.[CrossRef][Medline]

MCCLINTOCK, B., 1945 Neurospora. I. Preliminary observations of the chromosomes of Neurospora crassa. Am. J. Bot. 32: 671–678.[CrossRef]

MYLYK, O. M., 1975 Heterokaryon incompatibility genes in Neurospora crassa detected using duplication-producing chromosome rearrangements. Genetics 80: 107–124.[Abstract/Free Full Text]

MYLYK, O. M., 1976 Heteromorphism for heterokaryon incompatibility genes in natural populations of Neurospora crassa. Genetics 83: 275–284.[Abstract/Free Full Text]

NEWMEYER, D., 1962 Genes influencing the conversion of citrulline to argininosuccinate in Neurospora crassa. J. Gen. Microbiol. 28: 215–230.[Medline]

NEWMEYER, D., and E. L. TATUM, 1953 Gene expression in Neurospora mutants requiring nicotinic acid or tryptophan. Am. J. Bot. 40: 393–400.[CrossRef]

PANDIT, A., and R. MAHESHWARI, 1996 Life-history of Neurospora intermedia in a sugar cane field. J. Biosci. 21: 57–79.[CrossRef]

PERKINS, D. D., 1994 How should the infertility of interspecies crosses be designated? Mycologia 86: 758–761.[CrossRef]

PERKINS, D. D., 1997 Chromosome rearrangements in Neurospora and other filamentous fungi. Adv. Genet. 36: 239–398.[Medline]

PERKINS, D. D., and E. G. BARRY, 1977 The cytogenetics of Neurospora. Adv. Genet. 19: 133–285.[Medline]

PERKINS, D. D., and N. B. RAJU, 1986 Neurospora discreta, a new heterothallic species defined by its crossing behavior. Exp. Mycol. 10: 323–338.[CrossRef]

PERKINS, D. D., and B. C. TURNER, 1988 Neurospora from natural populations: toward the population biology of a haploid eukaryote. Exp. Mycol. 12: 91–131.[CrossRef]

PERKINS, D. D., D. NEWMEYER, C. W. TAYLOR and D. C. BENNETT, 1969 New markers and map sequences in Neurospora crassa, with a description of mapping by duplication coverage and of multiple translocation stocks for testing linkage. Genetica 40: 247–278.[CrossRef][Medline]

PERKINS, D. D., B. C. TURNER and E. G. BARRY, 1976 Strains of Neurospora collected from nature. Evolution 30: 281–313.[CrossRef]

PERKINS, D. D., A. RADFORD and M. S. SACHS, 2001 The Neurospora Compendium: Chromosomal Loci. Academic Press, San Diego.

PERKINS, D. D., M. FREITAG, V. C. POLLARD, L. A. BAILEY-SHRODE, E. U. SELKER et al., 2007 Recurrent locus-specific mutation resulting from a cryptic ectopic insertion in Neurospora. Genetics 175: 527–544.[Abstract/Free Full Text]

POWELL, A. J., D. J. JACOBSON, L. SALTER and D. O. NATVIG, 2003 Variation among natural isolates of Neurospora on small spatial scales. Mycologia 95: 809–819.[Abstract/Free Full Text]

RAJU, N. B., 1992 Genetic control of the sexual cycle in Neurospora. Mycol. Res. 96: 241–262.

RAJU, N. B., 2002 Spore killers: meiotic drive elements that distort genetic ratios, pp. 275–296 in Molecular Biology of Fungal Development, edited by H. D. OSIEWACZ. Marcel Dekker, New York.

SELKER, E. U., 1999 Gene silencing: repeats that count. Cell 97: 157–160.[CrossRef][Medline]

SHEAR, C. L., and B. O. DODGE, 1927 Life histories and heterothallism of the red bread-mold fungi of the Monilia sitophila group. J. Agric. Res. 34: 1019–1042.

SHIU, P. K., N. B. RAJU, D. ZICKLER and R. L. METZENBERG, 2001 Meiotic silencing by unpaired DNA. Cell 107: 905–916.[CrossRef][Medline]

SINGLETON, J. R., 1953 Chromosome morphology and the chromosome cycle in the ascus of Neurospora crassa. Am. J. Bot. 40: 124–144.[CrossRef]

SKUPSKI, M. P., D. A. JACKSON and D. O. NATVIG, 1997 Phylogenetic analysis of heterothallic Neurospora species. Fungal Genet. Biol. 21: 153–162.[CrossRef][Medline]

SPIETH, P. T., 1975 Population genetics of allozyme variation in Neurospora intermedia. Genetics 80: 785–805.[Abstract/Free Full Text]

TURNER, B. C., 2001 Geographical distribution of Spore killer meiotic drive strains and of strains resistant to killing in Neurospora. Fungal Genet. Biol. 32: 93–104.[CrossRef][Medline]

TURNER, B. C., and D. D. PERKINS, 1979 Spore killer, a chromosomal factor in Neurospora that kills meiotic products not containing it. Genetics 93: 587–606.[Abstract/Free Full Text]

TURNER, B. C., D. D. PERKINS and A. FAIRFIELD, 2001 Neurospora from natural populations: a global study. Fungal Genet. Biol. 32: 67–92.[CrossRef][Medline]

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