scholarly journals SiSTL1, encoding a large subunit of ribonucleotide reductase, is crucial for plant growth, chloroplast biogenesis, and cell cycle progression in Setaria italica

2018 ◽  
Vol 70 (4) ◽  
pp. 1167-1182
Author(s):  
Chanjuan Tang ◽  
Sha Tang ◽  
Shuo Zhang ◽  
Mingzhao Luo ◽  
Guanqing Jia ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Plant Growth ◽  
Ribonucleotide Reductase ◽  
Cell Cycle Progression ◽  
Large Subunit ◽  
Setaria Italica ◽  
Chloroplast Biogenesis ◽  
Cycle Progression

scholarly journals Requirement and functional redundancy of two large ribonucleotide reductase subunit genes for cell cycle, chloroplast biogenesis in tomato

2020 ◽  
Author(s):  
Mengjun Gu ◽  
Yi Liu ◽  
Man Cui ◽  
Huilan Wu ◽  
Hong-Qing Ling
Keyword(s):  
Cell Cycle ◽  
Ribonucleotide Reductase ◽  
Cell Cycle Progression ◽  
De Novo ◽  
Large Subunit ◽  
Chloroplast Biogenesis ◽  
Tomato Genome ◽  
Cycle Progression ◽  
Tomato Growth ◽  
Regulation Of Cell Cycle

AbstractRibonucleotide reductase (RNR), functioning in the de novo synthesis of dNTPs, is crucial for DNA replication and cell cycle progression. However, the knowledge about the RNR in plants is still limited. In this study, we isolated ylc1 (young leaf chlorosis 1) mutant, which exhibited many development defects such as dwarf stature, chlorotic young leaf, and smaller fruits. Map-based cloning, complementation, and knocking-out experiments confirmed that YLC1 encodes a large subunit of RNR (SlRNRL1), an enzyme involved in the de novo biosynthesis of dNTPs. Physiological and transcriptomic analyses indicate that SlRNRL1 plays a crucial role in the regulation of cell cycle, chloroplast biogenesis, and photosynthesis in tomato. In addition, we knocked out SlRNRL2 (a SlRNRL1 homolog) using CRISPR-Cas9 technology in the tomato genome, and found that SlRNRL2, possessing a redundant function with SlRNRL1, played a weak role in the formation of RNR complex due to its low expression intensity. Genetic analysis reveals that SlRNRL1 and SlRNRL2 are essential for tomato growth and development as the double mutant slrnrl1slrnrl2 is lethal. This also implies that the de novo synthesis of dNTPs is required for seed development in tomato. Overall, our results provide a new insight for understanding the SlRNRL1 and SlRNRL2 functions and the mechanism of de novo biosynthesis of dNTPs in plants.

scholarly journals Phytosulfokine-.ALPHA., a Peptidyl Plant Growth Factor, Stimulates Cell Cycle Progression in Carrot Non-Embryogenic Cells.

2003 ◽  
Vol 20 (3) ◽  
pp. 195-205 ◽  
Author(s):  
Chang-Ho EUN ◽  
Suk-Min KO ◽  
Katsumi HIGASHI ◽  
Dennis YEO ◽  
Yoshikatsu MATSUBAYASHI ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Growth Factor ◽  
Plant Growth ◽  
Cell Cycle Progression ◽  
Cycle Progression ◽  
Embryogenic Cells

Mutations in the large subunit of U2AF disrupt pre-mRNA splicing, cell cycle progression and nuclear structure

Yeast ◽  
2000 ◽  
Vol 16 (11) ◽  
pp. 1001-1013 ◽  
Author(s):  
Mitchell Beales ◽  
Nina Flay ◽  
Ron McKinney ◽  
Yasuaki Habara ◽  
Yasumi Ohshima ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Nuclear Structure ◽  
Cell Cycle Progression ◽  
Large Subunit ◽  
Mrna Splicing ◽  
Cycle Progression

Developmental control of a G1-S transcriptional program in Drosophila

Development ◽  
1994 ◽  
Vol 120 (6) ◽  
pp. 1503-1515 ◽  
Author(s):  
R.J. Duronio ◽  
P.H. O'Farrell
Keyword(s):  
Cell Cycle ◽  
Ribonucleotide Reductase ◽  
Temporal Pattern ◽  
Cell Cycle Progression ◽  
S Phase ◽  
Transcriptional Program ◽  
Cycle Progression ◽  
Dna Polymerase Alpha ◽  
Secondary Consequence ◽  
Drosophila Embryos

We have defined a coordinate program of transcription of S-phase genes (DNA polymerase alpha, PCNA and the two ribonucleotide reductase subunits) that can be induced by the G1 cyclin, cyclin E. In Drosophila embryos, this program drives an intricate spatial and temporal pattern of gene expression that perfectly parallels the embryonic program of S-phase control. This dynamic pattern of expression is not disrupted by a mutation, string, that blocks the cell cycle. Thus, the transcriptional program is not a secondary consequence of cell cycle progression. We suggest that developmental signals control this transcriptional program and that its activation either directly or indirectly drives transition from G1 to S phase in the stereotyped embryonic pattern.

The potential of iron chelators of the pyridoxal isonicotinoyl hydrazone class as effective antiproliferative agents, IV: the mechanisms involved in inhibiting cell-cycle progression

Blood ◽  
2001 ◽  
Vol 98 (3) ◽  
pp. 842-850 ◽  
Author(s):  
Jin Gao ◽  
Des R. Richardson
Keyword(s):  
Cell Cycle ◽  
Ribonucleotide Reductase ◽  
Cell Cycle Progression ◽  
Cell Cycle Control ◽  
Susceptibility Gene ◽  
Cycle Progression ◽  
Protein Levels ◽  
Ribonucleotide Reductase Inhibitor ◽  
Appreciable Increase ◽  
Pyridoxal Isonicotinoyl Hydrazone

Abstract Some chelators of the pyridoxal isonicotinoyl hydrazone class have antiproliferative activity that is far greater than desferrioxamine (DFO). In this study, DFO was compared with one of the most active chelators (311) on the expression of molecules that play key roles in cell-cycle control. This was vital for understanding the role of iron (Fe) in cell-cycle progression and for designing chelators to treat cancer. Incubating cells with DFO, and especially 311, resulted in a decrease in the hyperphosphorylated form of the retinoblastoma susceptibility gene product (pRb). Chelators also decreased cyclins D1, D2, and D3, which bind with cyclin-dependent kinase 4 (cdk4) to phosphorylate pRb. The levels of cdk2 also decreased after incubation with DFO, and especially 311, which may be important for explaining the decrease in hyperphosphorylated pRb. Cyclins A and B1 were also decreased after incubation with 311 and, to a lesser extent, DFO. In contrast, cyclin E levels increased. These effects were prevented by presaturating the chelators with Fe. In contrast to DFO and 311, the ribonucleotide reductase inhibitor hydroxyurea increased the expression of all cyclins. Hence, the effect of chelators on cyclin expression was not due to their ability to inhibit ribonucleotide reductase. Although chelators induced a marked increase in WAF1 and GADD45 mRNA transcripts, there was no appreciable increase in their protein levels. Failure to translate these cell-cycle inhibitors may contribute to dysregulation of the cell cycle after exposure to chelators.

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