Mutation in the prp12 + gene encoding a homolog of SAP130/SF3b130 causes differential inhibition of pre-mRNA splicing and arrest of cell-cycle progression in Schizosaccharomyces pombe

Abstract The prp (pre-mRNA processing) mutants of the fission yeast Schizosaccharomyces pombe have a defect in pre-mRNA splicing and accumulate mRNA precursors at a restrictive temperature. One of the prp mutants, prp1-4, also has a defect in poly(A)+ RNA transport. The prp1 + gene encodes a protein of 906 amino acid residues that contains 19 repeats of 34 amino acids termed tetratrico peptide repeat (TPR) motifs, which were proposed to mediate protein-protein interactions. The amino acid sequence of Prplp shares 29.6% identity and 50.6% similarity with that of the PRP6 protein of Saccharomyces cerevisiae, which is a component of the U4/U6 snRNP required for spliceosome assembly. No functional complementation was observed between S. pombe prp1 + and S. cerevisiae PRP6. We examined synthetic lethality of prp1-4 with the other known prp mutations in S. pombe. The results suggest that Prp1p interacts either physically or functionally with Prp4p, Prp6p and Prp13p. Interestingly, the prp1 + gene was found to be identical with the zer1 + gene that functions in cell cycle control. These results suggest that Prp1p/Zer1p is either directly or indirectly involved in cell cycle progression and/or poly(A)+ RNA nuclear export, in addition to pre-mRNA splicing.

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Structure of the human TIMP-3 gene and its cell cycle-regulated promoter

Biochemical Journal ◽

10.1042/bj3110549 ◽

1995 ◽

Vol 311 (2) ◽

pp. 549-554 ◽

Cited By ~ 37

Author(s):

M Wick ◽

R Härönen ◽

D Mumberg ◽

C Bürger ◽

B R Olsen ◽

...

Keyword(s):

Cell Cycle ◽

Cell Cycle Progression ◽

Alternative Polyadenylation ◽

Regulatory Elements ◽

Detailed Knowledge ◽

Gene Encoding ◽

Cycle Progression ◽

Physiological Processes ◽

Cycle Regulation

The gene encoding tissue inhibitor of metalloproteinases-3 (TIMP-3) is regulated during development, mitogenic stimulation and normal cell cycle progression. The TIMP-3 gene is structurally altered or deregulated in certain diseases of the eye and in tumour cells. A detailed knowledge of the TIMP-3 gene and its regulatory elements is therefore of paramount importance to understand its role in development, cell cycle progression and disease. In this study, we present the complete structure of the human TIMP-3 gene. We show that TIMP-3 is a TATA-less gene, which initiates transcription at one major site, is composed of five exons and four introns spanning a region of approximately 30 kb, and gives rise to three distinct mRNAs, presumably due to the usage of alternative polyadenylation signals. Using somatic cell hybrids the TIMP-3 locus was mapped to chromosomal location 22q13.1 We also show that the TIMP-3 5′ flanking region is sufficient to confer both high basal level expression in growing cells and cell cycle regulation in serum-stimulated cells. While the first 112 bases of the promoter, which harbour multiple Sp1 sites, were found to suffice for high basal level activity, the adjacent region spanning positions -463 and -112 was found to be a major determinant of serum inducibility. These results provide an important basis for further investigations addressing the role of TIMP-3 in physiological processes and pathological conditions.

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Functional analyses of interacting factors involved in both pre-mRNA splicing and cell cycle progression in Saccharomyces cerevisiae

RNA ◽

10.1017/s1355838200000984 ◽

2000 ◽

Vol 6 (11) ◽

pp. 1565-1572 ◽

Cited By ~ 36

Author(s):

CAROLINE S. RUSSELL ◽

SIGAL BEN-YEHUDA ◽

IAN DIX ◽

MARTIN KUPIEC ◽

JEAN D. BEGGS

Keyword(s):

Saccharomyces Cerevisiae ◽

Cell Cycle ◽

Cell Cycle Progression ◽

Mrna Splicing ◽

Cycle Progression ◽

Functional Analyses

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The role of proteolysis in cell cycle progression in Schizosaccharomyces pombe.

The EMBO Journal ◽

10.1002/j.1460-2075.1996.tb00912.x ◽

1996 ◽

Vol 15 (19) ◽

pp. 5268-5279 ◽

Cited By ~ 104

Author(s):

H. Yamano ◽

J. Gannon ◽

T. Hunt

Keyword(s):

Cell Cycle ◽

Schizosaccharomyces Pombe ◽

Cell Cycle Progression ◽

Cycle Progression

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Dynamic SUMO modification regulates mitotic chromosome assembly and cell cycle progression in Caenorhabditis elegans

Nature Communications ◽

10.1038/ncomms6485 ◽

2014 ◽

Vol 5 (1) ◽

Cited By ~ 31

Author(s):

Federico Pelisch ◽

Remi Sonneville ◽

Ehsan Pourkarimi ◽

Ana Agostinho ◽

J. Julian Blow ◽

...

Keyword(s):

Cell Cycle ◽

Caenorhabditis Elegans ◽

Cell Cycle Progression ◽

Metaphase Plate ◽

Gene Encoding ◽

Cycle Progression ◽

Sumo Protease ◽

Sumo Conjugation ◽

Centromeric Protein ◽

Cycle Regulation

Abstract The small ubiquitin-like modifier (SUMO), initially characterized as a suppressor of a mutation in the gene encoding the centromeric protein MIF2, is involved in many aspects of cell cycle regulation. The dynamics of conjugation and deconjugation and the role of SUMO during the cell cycle remain unexplored. Here we used Caenorhabditis elegans to establish the contribution of SUMO to a timely and accurate cell division. Chromatin-associated SUMO conjugates increase during metaphase but decrease rapidly during anaphase. Accumulation of SUMO conjugates on the metaphase plate and proper chromosome alignment depend on the SUMO E2 conjugating enzyme UBC-9 and SUMO E3 ligase PIASGEI-17. Deconjugation is achieved by the SUMO protease ULP-4 and is crucial for correct progression through the cell cycle. Moreover, ULP-4 is necessary for Aurora BAIR-2 extraction from chromatin and relocation to the spindle mid-zone. Our results show that dynamic SUMO conjugation plays a role in cell cycle progression.

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Incompatibility between proliferation and plant invasion is mediated by a regulator of appressorium formation in the corn smut fungusUstilago maydis

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.2006909117 ◽

2020 ◽

Vol 117 (48) ◽

pp. 30599-30609

Author(s):

Antonio de la Torre ◽

Sónia Castanheira ◽

José Pérez-Martín

Keyword(s):

Cell Cycle ◽

Cell Cycle Progression ◽

Pathogenic Fungi ◽

Phytopathogenic Fungi ◽

Toggle Switch ◽

Appressorium Formation ◽

M Cell ◽

Gene Encoding ◽

Cycle Progression ◽

Corn Smut

Plant pathogenic fungi often developed specialized infection structures to breach the outer surface of a host plant. These structures, called appressoria, lead the invasion of the plant by the fungal hyphae. Studies in different phytopathogenic fungi showed that appressorium formation seems to be subordinated to the cell cycle. This subordination ensures the loading in the invading hypha of the correct genetic information to proceed with plant infection. However, how the cell cycle transmits its condition to the genetic program controlling appressorium formation and promoting the plant’s invasion is unknown. Our results have uncovered how this process occurs for the appressorium ofUstilago maydis, the agent responsible for corn smut disease. Here, we described that the complex Clb2-cyclin-dependent kinase (Cdk)1, one of the master regulators of G2/M cell cycle progression inU. maydis, interacts and controls the subcellular localization of Biz1, a transcriptional factor required for the activation of the appressorium formation. Besides, Biz1 can arrest the cell cycle by down-regulation of the gene encoding a second b-cyclin Clb1 also required for the G2/M transition. These results revealed a negative feedback loop between appressorium formation and cell cycle progression inU. maydis, which serves as a “toggle switch” to control the fungal decision between infecting the plant or proliferating out of the plant.

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