Anaphase-promoting complex/cyclosome （APC/C）, a multisubunit E3 ligase, plays a critical role in cell cycle control, but the functional characterization of each subunit has not yet been completed. To investigate the...Anaphase-promoting complex/cyclosome （APC/C）, a multisubunit E3 ligase, plays a critical role in cell cycle control, but the functional characterization of each subunit has not yet been completed. To investigate the function of APC1 in Arabidopsis, we analyzed four mutant alleles of APC1, and found that mutation in APC1 resulted in significantly reduced plant fertility, accumulation of cyclin B, and disrupted auxin distribution in embryos. The three mutant alleles apcl-1, apcl-2 and apcl-3 shared variable defects in female gametogenesis including degradation, abnormal nuclear number, and disrupted polarity of nuclei in the embryo sac as well as in embryogenesis, in which embryos were arrested at multiple stages. All of these defects are similar to those previously identified in apc4. The mutant apcl-4, in which the T-DNA was inserted after the transmembrane domain at the C-terminus, showed much more severe phenotypes; that is, most of the ovules were arrested at the one-nucleate female gametophyte stage （stage FG1）. In the apcl apc4 double mutants, the fertility was further reduced by one-third in apcl-ll＋ apc4-1/＋, and in some cases no ovules even survived in siliques of apcl-4/＋ apc4-1/＋. Our data thus suggest that APC1, an essential component of APC/C, plays a synergistic role with APC4 both in female gametogenesis and in embryogenesis.展开更多
基金supported by the National Key Basic Research Program of the People’s Republic of China (2012CB944801 and 2011CB915402)the National Science Foundation of China(30970270 to J.J.L.)
文摘Anaphase-promoting complex/cyclosome （APC/C）, a multisubunit E3 ligase, plays a critical role in cell cycle control, but the functional characterization of each subunit has not yet been completed. To investigate the function of APC1 in Arabidopsis, we analyzed four mutant alleles of APC1, and found that mutation in APC1 resulted in significantly reduced plant fertility, accumulation of cyclin B, and disrupted auxin distribution in embryos. The three mutant alleles apcl-1, apcl-2 and apcl-3 shared variable defects in female gametogenesis including degradation, abnormal nuclear number, and disrupted polarity of nuclei in the embryo sac as well as in embryogenesis, in which embryos were arrested at multiple stages. All of these defects are similar to those previously identified in apc4. The mutant apcl-4, in which the T-DNA was inserted after the transmembrane domain at the C-terminus, showed much more severe phenotypes; that is, most of the ovules were arrested at the one-nucleate female gametophyte stage （stage FG1）. In the apcl apc4 double mutants, the fertility was further reduced by one-third in apcl-ll＋ apc4-1/＋, and in some cases no ovules even survived in siliques of apcl-4/＋ apc4-1/＋. Our data thus suggest that APC1, an essential component of APC/C, plays a synergistic role with APC4 both in female gametogenesis and in embryogenesis.
