1 U. maydis deploys many effector proteins to manipulate i
2 In S. cerevisiae
and U. maydis, NPC motility prevented NPCs from clustering.
3 to 5 transformants/micrograms linear DNA
and U. maydis at up to 25 transformants/microgram circular D
4 icity, are very similar in P. flocculosa
and U. maydis, Sporisorium reilianum, and Ustilago hordei.
5 ystatin (CC9) is induced upon penetration
by U. maydis wild type.
6 nt double-stranded RNA (dsRNA) virus in
each U. maydis subtype.
7 For U. maydis, disruption of ump2 eliminated the filamentous
8 The two genes
from U. maydis and one of the genes from M. violaceum were ex
9 errichrome and ferrichrome A biosynthesis
in U. maydis.
10 e pheromone-responsive MAP kinase cascade
in U. maydis.
11 s of filamentous growth and pathogenicity
in U. maydis.
12 ontrol of morphogenesis and pathogenicity
in U. maydis.
13 ole in the recombinational repair pathway
in U. maydis, and imply that it plays a similar key role in
14 DNA repair and recombination proficiency
in U. maydis requires both Rec2 and Rad51.
15 Recapitulation
in U. maydis of defects in DNA repair and genome stability
16 These results indicate that gap repair
in U. maydis is unlikely to proceed by the mechanism envisi
17 asis for the extreme radiation resistance
in U. maydis.
18 Studies
in U. maydis and Aspergillus nidulans reveal a complex inte
19 efficient homologous recombination system
in U. maydis.
20 Our findings suggest that
in U. maydis, unprotected telomeres arising from Ku depleti
21 re three well-characterized killer toxins
in U. maydis-KP1, KP4, and KP6-which are secreted by the P1
22 emonstrate that KP4 affects (45)Ca uptake
in U. maydis.
23 proteins reported to influence virulence
in U. maydis as the singular divergence that could explain
24 t, NPC motility required F-actin, whereas
in U. maydis, microtubules, kinesin-1, and dynein drove por
25 Mutants
of U. maydis deleted of DSS1 are extremely radiation sensit
26 e phenotypes mirror previous observations
of U. maydis mutants deficient in Brh2 or Rad51.
27 Phenotypic screening
of U. maydis mutants deleted for genes encoding secreted pr
28 olution of a system enabling the survival
of U. maydis under such conditions could be a secondary con
29 nteraction of maize with the fungal
pathogen U. maydis.
30 In telomerase-
positive U. maydis, deletion of rad51 and blm separately caused s
31 confirm and extend earlier observations
that U. maydis hyphae branch extensively on the leaf surface
32 The U. maydis killer toxin KP6 contains two polypeptide chai
33 d in genome defense, that are lacking in
the U. maydis genome due to clean excision events.
34 ranslocation of a number of effectors in
the U. maydis-maize system and show data that suggest that t
35 Moreover,
the U. maydis ump2 gene, initially detected as an upregulate
36 The unusual C-terminal extension of
the U. maydis Hac1 homolog, Cib1 (for Clp1 interacting bZIP1
37 romoter and iron-regulatory sequences of
the U. maydis sid1 gene were defined by fusing restriction a
38 Here, we show that
the U. maydis class VII chitin synthase and 1,3-beta-glucan
39 cc9 is not induced after infection with
the U. maydis effector mutant Deltapep1, which elicits massi
40 in lignin biosynthesis are hypersensitive
to U. maydis infection.
41 expression and a hypersensitive response
to U. maydis wild-type infection.
42 While U. maydis Deltagls1 cells induce strong plant defense re