EC Number   |
General Information |
Reference |
|---|
   3.1.21.10 | malfunction |
deletion of the enzyme leads to delay in DNA synthesis |
730710 |
| 3.1.21.10 | malfunction |
enzyme depletion induces ectopic recombination between short dispersed repeats in plastidial DNA and disorganizes thylakoid membranes in plastid |
762166 |
| 3.1.21.10 | malfunction |
enzyme depletion results in the appearance of cells with compact nucleoids, septa formed over the DNA and anucleate cells. Enzyme-depleted cells also show increased septal recruitment of the DNA translocase SpoIIIE, presumably to resolve chromosome segregation defects. Additionally cells are more sensitive to DNA damaging agents such as mitomycin C or UV radiation |
-, 729501 |
| 3.1.21.10 | malfunction |
gen-1 mutants are defective in DNA damage-dependent cell cycle arrest and apoptosis and in positional cloning of GEN-1, phenotypes, detailed overview |
716664 |
| 3.1.21.10 | malfunction |
GEN1 depletion results in aberrant centrosome numbers associated with the formation of multiple spindle poles in mitosis, an increased number of cells with multi-nuclei, increased apoptosis and an elevated level of spontaneous DNA damage |
730712 |
| 3.1.21.10 | malfunction |
loss of Mus81 activity sensitizes yeast cells to a large panel of agents whose effects inhibit RF progression, including methyl methanesulfonate, UV light, camptothecin, hydroxyurea, and DNA cross-linking agents |
729606 |
| 3.1.21.10 | malfunction |
mutations at the Cre04.g218000 gene are responsible for the mocH72 phenotype and with monokaryotic chloroplasts, which possess only a single chloroplast nucleoid and show unequal segregation of chloroplast nucleoids during chloroplast divisions |
752259 |
| 3.1.21.10 | malfunction |
reduced or no expression of MOC1 in Arabidopsis thaliana leads to growth defects and aberrant chloroplast nucleotide segregation |
752259 |
| 3.1.21.10 | malfunction |
single mutants of hjc and hef display no significant defects in growth or homologous recombination. Deletion of hef confers only moderate sensitivity to DNA crosslinking agents, whereas mutation of FANCM in leads to hypersensitivity in eukaryotes. Absence of hef or hjc leads to growth defects in presence of mitomycin C, deletion of both leads to synthetic lethality |
714816 |
| 3.1.21.10 | malfunction |
strains lacking RuvABC are inviable and accumulate Holliday junctions that interfere with growth and division of the cells |
715117 |
