000			02122nab|a22003497a|4500
001			64702
003			MX-TxCIM
005			20211213160559.0
008			202003s2019||||xxk|||p|op||||00||0|eng|d
022			_a2050-084X
024	8		_ahttps://doi.org/10.7554/eLife.48943
040			_aMX-TxCIM
041			_aeng
100	1		_aBardetti, P. _925910
245	1	0	_aCytoplasmic retention and degradation of a mitotic inducer enable plant infection by a pathogenic fungus
260			_aCambridge : _beLife Sciences Publications, _c2019.
500			_aPeer review
500			_aOpen Access
520			_aIn the fungus Ustilago maydis, sexual pheromones elicit mating resulting in an infective filament able to infect corn plants. Along this process a G2 cell cycle arrest is mandatory. Such as cell cycle arrest is initiated upon the pheromone recognition in each mating partner, and sustained once cell fusion occurred until the fungus enter the plant tissue. We describe that the initial cell cycle arrest resulted from inhibition of the nuclear transport of the mitotic inducer Cdc25 by targeting its importin, Kap123. Near cell fusion to take place, the increase on pheromone signaling promotes Cdc25 degradation, which seems to be important to ensure the maintenance of the G2 cell cycle arrest to lead the formation of the infective filament. This way, premating cell cycle arrest is linked to the subsequent steps required for establishment of the infection. Disabling this connection resulted in the inability of fungal cells to infect plants.
546			_aText in English
591			_aBentley, A.R. : No CIMMYT Affiliation
650		7	_aUstilago zeae _2AGROVOC _99188
650		7	_aCell cycle _2AGROVOC _913512
650		7	_aPathogenic fungi _2AGROVOC _913425
700	1		_aCastanheira, S.M. _925911
700	1		_aValerius, O. _925912
700	1		_aBraus, G.H. _925913
700	1		_aPérez-Martín, J. _925914
773	0		_teLife _gv. 8, e48943 _dCambridge : eLife Sciences Publications, 2019. _x2050-084X
856	4		_yClick here to access online _uhttps://doi.org/10.7554/eLife.48943
942			_cJA _n0 _2ddc
999			_c64702 _d64694