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Learn More. Mating-type switching is a complex mechanism that promotes sexual reproduction in Saccharomycotina.

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The reasons why all the elements of the mating-type switching system have been conserved in some Saccharomycotina, that do not show a sexual cycle nor mating-type switching, remain unknown. To gain insight on this phenomenon, we used the yeast Candida glabrataphylogenetically close to S.

We have ly shown that expression of S. To understand the link between mating-type switching and cell death in C. We demonstrate that mating-type switching in C. We also show that switching is Raddependent, as in S. Mating-type switching is one of the strategies developed by fungi to promote sexual reproduction and propagation.

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This mechanism enables one haploid cell to give rise to a cell of the opposite mating-type so that they can mate. It has been extensively studied in the yeast S. Little is known about why the mating-type switching components have been conserved in species like C. We have ly shown that mating-type switching can be triggered, in C. In this work, we show that mating-type switching in C. We demonstrate that the cut at MAT is only lethal when the Ho endonuclease performs the break, a situation unique to C. Our work points to a degeneration of the mating-type switching system in C.

Further studies of this phenomenon should shed light on the evolution of mating systems in asexual yeasts.

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In eukaryotes, sexual reproduction is a nearly ubiquitous feature and implies fundamental conserved processes such as gamete fusion, zygote formation and meiosis [ 1 ]. Sexual reproduction le to genetic recombination between organisms and thus enables them to purge their genomes from deleterious mutations, as well as to increase their genetic diversity.

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It is in the fungal kingdom that the greatest diversity of sexual reproduction is found [ 1 ]. Particularly, sexual reproduction in fungal pathogens of human exhibits a considerable plasticity between species [ 23 ]. While many were thought to be asexual, several atypical sexual or parasexual cycles have been discovered.

It has been shown that the yeast Candida albicans can perform a parasexual cycle by mating of two diploid cells, forming a tetraploid, that can undergo chromosome loss [ 4 ]. The more distant filamentous opportunistic pathogen, Aspergillus fumigatus exhibits a sexual cycle but only mates after spending 6—12 months in the dark [ 5 ].

Altogether, this suggests that, in most fungi, performing genetic exchange is crucial, even in well-adapted human pathogens. In fungi, sexual reproduction can occur through three mechanisms [ 1 ]: heterothallism requiring two compatible partners for mating to occurhomothallism self-fertilityand pseudo-homothallism where a single individual can go through a complete sexual cycle but mating only occurs between two compatible partners.

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Pseudo-homothallism has mainly been described in ascomycete yeasts where it occurs through a programmed differentiation process called mating-type switching [ 6 ]. In all cases studied so far, it implies a genomic DNA rearrangement of the mating-type locus MATencoding the key regulators of sexual identity and species have evolved very different molecular pathways for the same aim. In the fission yeast Schizosaccharomyces pombean imprint at mat1 it is unknown whether the imprint is an epigenetic mark or a single nick is introduced, that le to a DSB during DNA replication [ 78 ].

Repair occurs with one of the two silent copies of mat1called mat2 and mat3. In the ascomycete Kluyveromyces lactismating-type switching involves a DSB at MAT but it is performed by two specific nucleases depending on the mating-type of the cell [ 910 ]. Mating-type switching has been extensively studied in the model yeast S.

DSBs are highly toxic DNA lesions, and thus have to be efficiently repaired to ensure cell viability. This can be achieved through two major pathways, non-homologous end-ing NHEJ and homologous recombination HR in the presence of a repair template.

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It must be noted that the Ho recognition site is quite different between the "a" and "alpha" versions, one side is unchanged since it is located in the identical Z sequence, while the other side, corresponding to the end of the Y fragment, is different between the two mating-types Fig 1. There is no measurable difference in the efficacy of the cut between the two sequences, nor between efficiency of mating-type switching from one to another [ 1617 ].

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This illustrates the fact that Ho is part of the family of meganucleases, that do not function like type II restriction endonucleases, but recognize large larger than 12bpdegenerate, non-palindromic cut-sites. The Ho site sequence of each locus and species is shown in yellow.

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It must be noted that mating-type switching occurs only once per cell-cycle, in G1, and that this is thought to be regulated through the control of the expression of HO [ 12 ], but experiments of overexpression of HO under the control of a galactose-inducible promoter have shown that the switch can be induced in any part of the cell cycle [ 19 ]. Intriguingly, there is no report of switching back and forth between the two mating-types in such overexpression experiments, leaving open the possibility that another mechanism than HO gene expression, is responsible for the "unswitchability" of newly i.

The three loci display a structure comparable to S. Despite these similarities, added to the fact that both MATa and MATalpha cells are found naturally and that they maintain some mating-type identity [ 21 — 23 ], C. We have ly shown that the expression of the HO gene from S. We have also observed gene conversion events at the HML locus in survivors, revealing that, unlike S.

We suggested that the lethality was due to multiple chromosomal DSBs, which would prevent homologous recombination with an intact template in most cells.

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In this work, we investigate the reasons for the lethality associated with mating-type switching induced by Sc Ho. For this purpose, we constructed a series of inconvertible Inc C. We analyzed two aspects: viability, that reflects both the efficiency of the cut and the success of repair; and molecular structure of repaired loci, in wild-type and mutant strains, in order to reveal which repair pathways were used. In addition, by mimicking S. We expressed S. As ly described, expression of ScHO in wild-type strains of C.

Percentage of switch is calculated as the ratio of the total of pure and mixed colonies exhibiting mating-type switching divided by the total of surviving colonies tested, expressed as percentage. The square root of the of surviving colonies screened is used as standard error in last column.

Inducing the Ho DSB in this strain le to an even higher lethality than in the wild-type strain Fig 2and no mating-type switching is detected at any MTL locus Table 2confirming that switching relies on HR in C. On the left, diagram of MTL configuration of strains is shown with the corresponding survival histogram to Sc Ho induction on the right. The blue box represents the Ya, the red box Yalpha, the yellow bar wild-type Ho site and the crossed circle mutated Ho site Inc loci not to scale.

On the histogram, black bars are for strains from the BG87 background, grey bars are for strains from the HM background. for strains HM and BG87 are from Values from, at least, four experiments were averaged, the SEM used as estimate of the error and the P-value was calculated using the Wilcoxon test. As we hypothesized in our work [ 26 ], Ho-induced lethality in C. These unrepairable cuts would lead to death by cell cycle arrest, or because cut and possibly degraded chromosomes segregating into daughter cells lack essential genes.

Alternatively, we had mentioned the possibility that switching le to the repair of the Ho-cut locus by an intact Ho-site containing locus would cause never-ending cycles of cutting and repair that could also lead to cell death in our conditions of continuous induction on plates. We had dismissed this eventuality as unlikely, since the percentage of lethality and switched survivors is highly reproducible in our experiments.

Even though the situation is the same in S. We thus decided to de experiments which would address both the question of the of cut loci, and the question of the of cuts per locus. In these strains, we mutated the Ho sites in the region known to be essential for Ho cutting in S. This allows the distinction of the original HML or HMR locus from the repaired locus that has become resistant to cutting.

Upon Ho induction, we found that survival rate does not exceed 0.

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Once again, survival does not exceed 0. This reinforces the hypothesis that simultaneous DSBs, happening in wild-type strains, participate in the high lethality observed.

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Altogether, these suggest that the efficient Ho-cut at HML and HMR is not an important contributor to lethality in all configurations where they can be repaired by HR. In the absence of HR, no other mechanism such as NHEJ is able to take over the repair of the Ho-cut, and thus cell survival remains low. also show that protecting the MAT locus from the Ho-cut ificantly increases survival.

In order to measure the impact of the Ho cleavage at MAT on cell survival, we mimicked the situation in S. Furthermore, this experiment allows us to reconsider the question of lethality due to never-ending cycles of cutting and repair. Indeed, if this was the reason for mortality of cells when cutting at MATthen, since repairing with an Inc locus le to an unswitchable locus, the mortality should be decreased in these strains upon induction. Since we know that the mating-type switching system in C.

We asked whether such repair intermediates could be toxic and cause death. We analyzed the molecular structure in surviving colonies Table 2.

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It, therefore, seems unlikely that lethality could be due to non-resolvable HR intermediates. In order to shed light on whether the toxic effect leading to cell death could be reversible and if not, whether the effect operates rapidly or not, we performed a time course experiment in which Ho is induced in liquid medium and its expression is repressed, at different time points, by plating cells on repressive medium.

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The survival can thus be calculated by the ratio of colonies obtained on repressive medium to the theoretical of cells plated. This allows to follow a single Ho-cut and a single repair event at the MAT locus.