Evidence for a Pneumocystis carinii Flo8-like transcription factor: insights into organism adhesion

Kottom, Theodore J.; Limper, Andrew H.

doi:10.1007/s00430-015-0428-8

Cited by 7 publications

(7 citation statements)

References 45 publications

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“…The surface of P. carinii trophic cells was shown to harbor also the surface protein INT1 participating in adhesion ( 30 ). Recently, a transcription factor responsible for expression of a still unidentified adhesive surface protein (or proteins) has been reported in P. carinii trophic cells ( 31 ). Genes encoding orthologs of these two latter proteins are also present in the P. jirovecii genome (results not shown).…”

Section: Discussionmentioning

confidence: 99%

“…Genes encoding orthologs of these two latter proteins are also present in the P. jirovecii genome (results not shown). Moreover, Kottom and Limper ( 31 ) mentioned that other uncharacterized genes that are important in binding to mammalian hosts are present in the P. carinii genome. Thus, the structure of the P. jirovecii cell surface is made of a complex mixture of different proteins.…”

Section: Discussionmentioning

confidence: 99%

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Mechanisms of Surface Antigenic Variation in the Human Pathogenic Fungus Pneumocystis jirovecii

Schmid‐Siegert

Richard

Luraschi

et al. 2017

mBio

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Microbial pathogens commonly escape the human immune system by varying surface proteins. We investigated the mechanisms used for that purpose by Pneumocystis jirovecii. This uncultivable fungus is an obligate pulmonary pathogen that in immunocompromised individuals causes pneumonia, a major life-threatening infection. Long-read PacBio sequencing was used to assemble a core of subtelomeres of a single P. jirovecii strain from a bronchoalveolar lavage fluid specimen from a single patient. A total of 113 genes encoding surface proteins were identified, including 28 pseudogenes. These genes formed a subtelomeric gene superfamily, which included five families encoding adhesive glycosylphosphatidylinositol (GPI)-anchored glycoproteins and one family encoding excreted glycoproteins. Numerical analyses suggested that diversification of the glycoproteins relies on mosaic genes created by ectopic recombination and occurs only within each family. DNA motifs suggested that all genes are expressed independently, except those of the family encoding the most abundant surface glycoproteins, which are subject to mutually exclusive expression. PCR analyses showed that exchange of the expressed gene of the latter family occurs frequently, possibly favored by the location of the genes proximal to the telomere because this allows concomitant telomere exchange. Our observations suggest that (i) the P. jirovecii cell surface is made of a complex mixture of different surface proteins, with a majority of a single isoform of the most abundant glycoprotein, (ii) genetic mosaicism within each family ensures variation of the glycoproteins, and (iii) the strategy of the fungus consists of the continuous production of new subpopulations composed of cells that are antigenically different.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Mechanisms of Surface Antigenic Variation in the Human Pathogenic Fungus Pneumocystis jirovecii

Schmid‐Siegert

Richard

Luraschi

et al. 2017

mBio

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show abstract

“…The surface of P. carinii trophic cells was shown to harbour also the surface protein INT1 participating to adhesion (30). Recently, a transcription factor responsible for expression of (a) still unidentified adhesive surface protein(s) has been reported in P. carinii trophic cells (31). Genes encoding orthologs of these two latter proteins are also present in the P. jirovecii genome (results not shown).…”

Section: Discussionmentioning

confidence: 99%

“…Genes encoding orthologs of these two latter proteins are also present in the P. jirovecii genome (results not shown). Moreover, Kottom and Limper (31) mentioned that other uncharacterized genes which are important in binding to mammalian hosts are present in the P. carinii genome. Thus, the structure of P. jirovecii cell surface is made of a complex mixture of different proteins.…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of surface antigenic variation in the human pathogenic fungusPneumocystis jirovecii

Schmid‐Siegert

Richard

Luraschi

et al. 2017

Preprint

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Microbial pathogens commonly escape the human immune system by varying surface proteins. We investigated the mechanisms used for that purpose by Pneumocystis jirovecii. This uncultivable fungus is an obligate pulmonary pathogen which causes pneumonia in immuno-compromised individuals, a major life-threatening infection. Long-read PacBio sequencing was used to assemble a core of subtelomeres of a single P. jirovecii strain from a bronchoalveolar lavage fluid specimen of a single patient. A total of 113 genes encoding surface proteins were identified, including 28 pseudogenes. These genes formed a subtelomeric gene superfamily which included five families encoding adhesive GPI-anchored glycoproteins, and one family encoding excreted glycoproteins. Numerical analyses suggested that diversification of the glycoproteins relies on mosaic genes created by ectopic recombination, and occurs only within each family. DNA motifs suggested that all genes are expressed independently, except those of the family encoding the most abundant surface glycoproteins which are subject to mutually exclusive expression. PCR analyses showed that exchange of the expressed gene of the latter family occurs frequently, possibly favoured by the location of the genes proximal to the telomere because this allows concomitant telomere exchange. Our observations suggest that (i) P. jirovecii cell surface is made of a complex mixture of different surface proteins, with a majority of a single isoform of the most abundant glycoprotein, (ii) genetic mosaicism within each family ensures variation of the glycoproteins, and (iii) the strategy of the fungus consists in the continuous production of new subpopulations composed of cells which are antigenically different.

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“…It is assumed that these organisms possess a conventional transcription apparatus, since from database mining it is possible to find homologous genes encoding RNAPII subunits and GTFs. Furthermore, several transcriptional activators have been described in these organisms [ 16 , 17 ]. Stringer and colleagues have described two TBP genes from rat P. carinii and those gene products are highly identical in the conserved core with TBP polypeptides from other eukaryotic species [ 18 ].…”

Section: Introductionmentioning

confidence: 99%

RNA Polymerase II Transcription in Pneumocystis: TFIIB from Pneumocystis carinii Can Replace the Transcriptional Functions of Fission Yeast Schizosaccharomyces pombe TFIIB In Vivo and In Vitro

Rojas

Urbina

Solari

et al. 2022

IJMS

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The Pneumocystis genus is an opportunistic fungal pathogen that infects patients with AIDS and immunocompromised individuals. The study of this fungus has been hampered due to the inability to grow it in a (defined media/pure) culture. However, the use of modern molecular techniques and genomic analysis has helped researchers to understand its complex cell biology. The transcriptional process in the Pneumocystis genus has not been studied yet, although it is assumed that it has conventional transcriptional machinery. In this work, we have characterized the function of the RNA polymerase II (RNAPII) general transcription factor TFIIB from Pneumocystis carinii using the phylogenetically related biological model Schizosaccharomyces pombe. The results of this work show that Pneumocystis carinii TFIIB is able to replace the essential function of S. pombe TFIIB both in in vivo and in vitro assays. The S. pombe strain harboring the P carinii TFIIB grew slower than the parental wild-type S. pombe strain in complete media and in minimal media. The S. pombe cells carrying out the P. carinii TFIIB are larger than the wild-type cells, indicating that the TFIIB gene replacement confers a phenotype, most likely due to defects in transcription. P. carinii TFIIB forms very weak complexes with S. pombe TATA-binding protein on a TATA box promoter but it is able to form stable complexes in vitro when S. pombe TFIIF/RNAPII are added. P. carinii TFIIB can also replace the transcriptional function of S. pombe TFIIB in an in vitro assay. The transcription start sites (TSS) of the endogenous adh gene do not change when P. carinii TFIIB replaces S. pombe TFIIB, and neither does the TSS of the nmt1 gene, although this last gene is poorly transcribed in vivo in the presence of P. carinii TFIIB. Since transcription by RNA polymerase II in Pneumocystis is poorly understood, the results described in this study are promising and indicate that TFIIB from P. carinii can replace the transcriptional functions of S. pombe TFIIB, although the cells expressing the P. carini TFIIB show an altered phenotype. However, performing studies using a heterologous approach, like this one, could be relevant to understanding the basic molecular processes of Pneumocystis such as transcription and replication.

show abstract

Evidence for a Pneumocystis carinii Flo8-like transcription factor: insights into organism adhesion

Cited by 7 publications

References 45 publications

Mechanisms of Surface Antigenic Variation in the Human Pathogenic Fungus Pneumocystis jirovecii

Mechanisms of Surface Antigenic Variation in the Human Pathogenic Fungus Pneumocystis jirovecii

Mechanisms of surface antigenic variation in the human pathogenic fungusPneumocystis jirovecii

RNA Polymerase II Transcription in Pneumocystis: TFIIB from Pneumocystis carinii Can Replace the Transcriptional Functions of Fission Yeast Schizosaccharomyces pombe TFIIB In Vivo and In Vitro

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