scholarly journals RECESSIVE MUTATIONS FROM NATURAL POPULATIONS OF NEUROSPORA CRASSA THAT ARE EXPRESSED IN THE SEXUAL DIPLOPHASE

Genetics ◽  
1985 ◽  
Vol 111 (4) ◽  
pp. 759-777
Author(s):  
John F Leslie ◽  
Namboori B Raju

ABSTRACT Wild-collected isolates of Neurospora crassa Shear and Dodge were systematically examined for recessive mutations affecting the sexual phase of the life cycle, which is essentially diploid. Seventy-four of 99 wild-collected isolates from 26 populations in the United States, India and Pakistan carried one or more recessive mutations that reduced fertility significantly when homozygous; mutations affecting spore morphology were also detected. Limited complementation tests indicate that most of the 106 recovered mutations are unique.—The recessive diplophase (= sexual phase) mutations were uncovered by crossing each wild-collected isolate to a marked two-chromosome double-reciprocal translocation strain as "balancer." Surviving progeny receive approximately 60% of their genome from the wild parent, but receive the mating-type allele from the "balancer" parent. These progeny were backcrossed to the wild parent and were also crossed with a standard laboratory strain (fl). Reduced fertility in the backcross vs. normal fertility in the cross with the laboratory standard signals the presence of a recessive mutation in the wild-collected isolate.—Most of the mutants (95 of 106) fall into two major classes: those producing barren perithecia with no or few viable ascospores (51) and those with spore maturation defects (44). Most of the recessive barrens result either from an early block in meiosis or ascus development (25) or from a late disturbance in postmeiotic ascus behavior (18).—These recessive mutations are formally equivalent to recessive lethals in higher eukaryotes and may be important in determining the breeding structure of natural Neurospora populations.

Genome ◽  
1992 ◽  
Vol 35 (5) ◽  
pp. 815-826 ◽  
Author(s):  
Namboori B. Raju ◽  
John F. Leslie

Wild-collected strains of Neurospora crassa harbor recessive mutations that are expressed in the sexual phase when homozygous. Thirty-two representative mutants that produced barren perithecia were examined cytologically. Six of these mutants failed to form asci. Of the remaining 26, chromosome pairing was disturbed in 12 and meiosis was disturbed at pachytene or diplotene in 5. Seven mutants showed normal meiosis I but then diverged from the normal sequence, and two showed perithecial beak abnormalities. In many mutants, ascus development and nuclear divisions continued after the initial defect, albeit abnormally. Nuclear divisions were often delayed, essentially uncoupling them from other ascus events such as the formation of enlarged spindle pole body plaques, ascospore wall membranes, and spore delimitation. All 32 mutants were recessive and none showed obvious morphological abnormalities during vegetative growth. This phenotype contrasts sharply with that of numerous laboratory-induced ascus mutants, which are frequently expressed pleiotropically in the vegetative phase and several are dominant in the sexual phase.Key words: natural populations, sexual phase, recessive mutations, meiotic mutants, ascus development.


Genetics ◽  
1980 ◽  
Vol 96 (2) ◽  
pp. 435-454 ◽  
Author(s):  
H Robert Horvitz ◽  
John E Sulston

ABSTRACT Twenty-four mutants that alter the normally invariant post-embryonic cell lineages of the nematode Caenorhabditis elegans have been isolated and genetically characterized. In some of these mutants, cell divisions fail that occur in wild-type animals; in other mutants, cells divide that do not normally do so. The mutants differ in the specificities of their defects, so that it is possible to identify mutations that affect some cell lineages but not others. These mutants define 14 complementation groups, which have been mapped. The abnormal phenotype of most of the cell-lineage mutants results from a single recessive mutation; however, the excessive cell divisions characteristic of one strain, CB1322, require the presence of two unlinked recessive mutations. All 24 cell-lineage mutants display incomplete penetrance and/or variable expressivity. Three of the mutants are suppressed by pleiotropic suppressors believed to be specific for null alleles, suggesting that their phenotypes result from the complete absence of gene activity.


2021 ◽  
Author(s):  
Tomos Potter ◽  
Anja Felmy

AbstractIn wild populations, large individuals have disproportionately higher reproductive output than smaller individuals. We suggest an ecological explanation for this observation: asymmetry within populations in rates of resource assimilation, where greater assimilation causes both increased reproduction and body size. We assessed how the relationship between size and reproduction differs between wild and lab-reared Trinidadian guppies. We show that (i) reproduction increased disproportionately with body size in the wild but not in the lab, where effects of resource competition were eliminated; (ii) in the wild, the scaling exponent was greatest during the wet season, when resource competition is strongest; and (iii) detection of hyperallometric scaling of reproduction is inevitable if individual differences in assimilation are ignored. We propose that variation among individuals in assimilation – caused by size-dependent resource competition, niche expansion, and chance – can explain patterns of hyperallometric scaling of reproduction in natural populations.


Development ◽  
1992 ◽  
Vol 115 (1) ◽  
pp. 319-335 ◽  
Author(s):  
M. Jerka-Dziadosz ◽  
N. Garreau de Loubresse ◽  
J. Beisson

kin241 is a monogenic nuclear recessive mutation producing highly pleiotropic effects on cell size and shape, generation time, thermosensitivity, nuclear reorganization and cortical organization. We have analyzed the nature of the cortical disorders and their development during division, using various specific antibodies labelling either one of the cortical cytoskeleton components, as was previously done for analysis of cortical pattern formation in the wild type. Several abnormalities in basal body properties were consistently observed, although with a variable frequency: extra microtubules in either the triplets or in the lumen; nucleation of a second kinetodesmal fiber; abnormal orientation of the newly formed basal body with respect to the mother one. The latter effect seems to account for the major observed cortical disorders (reversal, intercalation of supplementary ciliary rows). The second major effect of the mutation concerns the spatiotemporal map of cortical reorganization during division. Excess basal body proliferation occurs and is correlated with modified boundaries of some of the cortical domains identified in the wild type on the basis of their basal body duplication pattern. This is the first mutant described in a ciliate in which both the structure and duplication of basal bodies and the body plan are affected. The data support the conclusion that the mutation does not alter the nature of the morphogenetic signal(s) which pervade the dividing cell, nor the competence of cytoskeletal structures to respond to signalling, but affects the local interpretation of the signals.


1989 ◽  
Vol 9 (10) ◽  
pp. 4259-4264
Author(s):  
B L Seidel-Rogol ◽  
J King ◽  
H Bertrand

The natural-death mutant of Neurospora crassa has an accelerated senescence phenotype caused by a recessive mutation, nd, in a nuclear gene that is located in linkage group I. An examination of mitochondrial functions, however, revealed that the mutant has phenotypic and molecular defects similar to those commonly associated with maternally transmitted fungal senescence syndromes, including (i) deficiencies in cytochromes aa3 and b; (ii) a deficit in small subunits of mitochondrial ribosomes, and hence defective mitochondrial protein synthesis; and (iii) accumulation of gross rearrangements, including large deletions, in the mitochondrial chromosome of vegetatively propagated cells. These traits indicate that the nd+ allele codes for a function that is essential for stable maintenance of the mitochondrial chromosome, possibly a protein involved in replication, repair, or recombination.


1989 ◽  
Vol 9 (10) ◽  
pp. 4259-4264 ◽  
Author(s):  
B L Seidel-Rogol ◽  
J King ◽  
H Bertrand

The natural-death mutant of Neurospora crassa has an accelerated senescence phenotype caused by a recessive mutation, nd, in a nuclear gene that is located in linkage group I. An examination of mitochondrial functions, however, revealed that the mutant has phenotypic and molecular defects similar to those commonly associated with maternally transmitted fungal senescence syndromes, including (i) deficiencies in cytochromes aa3 and b; (ii) a deficit in small subunits of mitochondrial ribosomes, and hence defective mitochondrial protein synthesis; and (iii) accumulation of gross rearrangements, including large deletions, in the mitochondrial chromosome of vegetatively propagated cells. These traits indicate that the nd+ allele codes for a function that is essential for stable maintenance of the mitochondrial chromosome, possibly a protein involved in replication, repair, or recombination.


2020 ◽  
Author(s):  
Martin Reichard ◽  
Radim Blažek ◽  
Jakub Žák ◽  
Petr Kačer ◽  
Oldřich Tomášek ◽  
...  

AbstractSex differences in lifespan and aging are widespread among animals, with males usually the shorter-lived sex. Despite extensive research interest, it is unclear how lifespan differences between the sexes are modulated by genetic, environmental and social factors. We combined comparative data from natural populations of annual killifishes with experimental results on replicated captive populations, showing that females consistently outlived males in the wild. This sex-specific survival difference persisted in social environment only in two most aggressive species, and ceased completely when social and physical contacts were prevented. Demographically, neither an earlier start nor faster rate of aging accounted for shorter male lifespans, but increased baseline mortality and the lack of mortality deceleration in the oldest age shortened male lifespan. The sexes did not differ in any measure of functional aging we recorded. Overall, we demonstrate that sex differences in lifespan and aging may be ameliorated by modulating social and environmental conditions.


Genetics ◽  
1978 ◽  
Vol 88 (4) ◽  
pp. 755-759
Author(s):  
Annie Fleuriet

ABSTRACT Polymorphism for both alleles of a gene ref(2)P, which is a usual trait of French natural populations of Drosophila melanogaster, can be reproduced in experimental conditions. ref(2)P is a gene for resistance to the hereditary, noncontagious Rhabdovirus α, responsible for CO2 sensitivity in Drosophila melanogaster. The equilibrium frequencies observed in cages are the same as in the wild, whether α virus is present or not. The rapid rate of return to these equilibrium frequencies indicates that strong forces, which remain to be determined, are responsible for the maintenance of this polymorphism.


Author(s):  
Donald Worster

In the wild garden of an early America there coiled and crawled the devil’s own plenty of poisonous vipers—cottonmouths, copperheads, coral snakes, the whole nasty family of rattlers and sidewinders. A naturalist roaming far from the settlements regularly ran the risk of a fatal snake bite. Fortunately, he was reassured by the field experts of the day, the deadly reptile always furnishes its own antidote. It conceals itself in the very plants whose roots can counteract its poison, plants like the so-called “Indian snakeroot.” As the viper sank its sharp fangs into your leg, you simply pulled up the roots of that plant, quickly chewed them down, and laughed in the viper’s face. You were instantly immune. How many backwoods naturalists and hunters died from believing that bit of advice is not known. Science, ever improving its hypotheses, now suggests carrying a snakebite kit in your pack or calling in a helicopter. But before we dismiss the old advice as completely foolish, we might ask whether it might not have had some useful, genuine logic in it. Sometimes the remedy for wounds does indeed lie near at hand among the shrubs and weeds in which the reptile lives; and sometimes dangerous forces do indeed suggest, or even contain, their own antidote. Take, for instance, the case of North America’s continuing environmental degradation. What we humans have done over the past five hundred years to maim this continent and tear apart its fabric of life is in large degree the consequence of the Judeo-Christian religious ethos and its modern secular offspring—science, industrial capitalism, and technology. I would put almost all the blame on the modern secular offspring, but I have to agree that religion too has been a deadly viper that has left its marks on the body of nature. Paradoxically, I would add what no one else seems to have noticed: an Indian snakeroot for this venom has appeared in the reptile’s own nest. The antidote for environmental destruction has been a movement called environmentalism and that movement has, in the United States, owed much of its program, temperament, and drive to the influence of Protestantism.


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Pallab Ghosh ◽  
Yan Zhou ◽  
Quentin Richardson ◽  
Darren E. Higgins

AbstractListeria monocytogenes is an intracellular pathogen responsible for listeriosis, a foodborne disease that can lead to life-threatening meningitis. The 2011 L. monocytogenes cantaloupe outbreak was among the deadliest foodborne outbreaks in the United States. We conducted in vitro and in vivo infection analyses to determine whether strains LS741 and LS743, two clinical isolates from the cantaloupe outbreak, differ significantly from the common laboratory strain 10403S. We showed that LS741 and LS743 exhibited increased virulence, characterized by higher colonization of the brain and other organs in mice. Assessment of cellular immune responses to known CD8+ T cell antigens was comparable between all strains. However, pre-existing immunity to 10403S did not confer protection in the brain against challenge with LS741. These studies provide insights into the pathogenesis of clinical isolates linked to the 2011 cantaloupe outbreak and also indicate that currently utilized laboratory strains are imperfect models for studying L. monocytogenes pathogenesis.


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