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1 atic conditions these species could maintain competitive fitness.
2 ompetitive fitness is similar to that of non-competitive fitness.
3 ecovery from nutrient downshift, and loss of competitive fitness.
4 n was dispensable for growth, virulence, and competitive fitness.
5 rom its contribution to Treg homeostasis and competitive fitness.
6 relation between mutations for body size and competitive fitness.
7 imals in order to survive and maximise their competitive fitness.
8  the PI3K-mTOR pathway increased mutant cell competitive fitness.
9  and patterns of recombination, and impaired competitive fitness.
10  resolving the genetic networks underpinning competitive fitness.
11 ific downstream factor regulating the GC-Tfh competitive fitness.
12 pecific aging-acquired mutations, may have a competitive fitness advantage after induction chemothera
13 at while the rpoS819 allele confers a strong competitive fitness advantage at basic pH, it confers a
14 ere that each of these polymerases confers a competitive fitness advantage during the stationary phas
15             RASA2-knockout CAR T cells had a competitive fitness advantage over control cells in the
16 henotype provided the evolved mutant phage a competitive fitness advantage over its ancestral wild-ty
17 the ability to induce cell death conferred a competitive fitness advantage to ST only during the acut
18           Moreover, the GAL lncRNAs confer a competitive fitness advantage to yeast cells because exp
19 etrieval during the recovery phase provide a competitive fitness advantage, likely promoting cell sur
20 formation, and the expansion of cells with a competitive fitness advantage.
21 nt against mutations affecting hermaphrodite competitive fitness agree to within two-fold, 0.33-0.5%.
22 AS locus are frequent in cancer and modulate competitive fitness and MEK dependency.
23  expression by CD8(+) T cells inhibits their competitive fitness and results in a slightly reduced ra
24             We find that Ppm1d regulates the competitive fitness and self-renewal of hematopoietic st
25 ubstitution enhances SARS-CoV-2 infectivity, competitive fitness, and transmission in primary human c
26                           Potential roles in competitive fitness are discussed.
27 al variance (VM) for male mating success and competitive fitness are not significantly different from
28                                         In a competitive fitness assay in human PC-3 tumors growing i
29 allowing us to pool the strains for in-vitro competitive fitness assays across 16 host-relevant antib
30                                              Competitive fitness assays of these pooled, barcoded, he
31                                              Competitive fitness assays show that aaim-1 mutants are
32 d in antimalarial concentration-response and competitive fitness assays.
33 ells resulted in their impaired function and competitive fitness, associated with markedly reduced CD
34 tes complex pools of barcoded mutants, whose competitive fitness can be measured during infection of
35                     When clones with similar competitive fitness collide, mutant cell fate reverts to
36 ains would be if these strains had increased competitive fitness compared to strains of other ribotyp
37 e viable but had no increased replication or competitive fitness compared to that of MHV-ExoN-AA.
38  resistance is universally associated with a competitive fitness cost and that this cost is determine
39 s identified priority access for Tregs and a competitive fitness cost of IL-2 production among both T
40 ance, implying mutants in this gene may have competitive fitness costs.
41  equal to the separately measured short-term competitive fitness deficit for the mismatch-repair-defi
42 heir natural environments where survival and competitive fitness depend upon both growth rate when co
43 ut also on the degree to which they generate competitive fitness differences.
44 ofilm-forming Bacillus subtilis and measured competitive fitness during colony co-culture with wild t
45 f bacillaene and other antibiotics optimizes competitive fitness for B. subtilis.
46 linked to pathophysiological and nutritional competitive fitness for survival in host tissues.
47 ere used to score complex phenotypes such as competitive fitness in a chemostat, DNA repair proficien
48 the non-cheaters and showed a high degree of competitive fitness in a human-derived consortium biofil
49 ltransferases were also required for maximum competitive fitness in and on leaves.
50 increases macrophage association and reduces competitive fitness in lungs, suggesting that ArgR influ
51 s more efficient infection, replication, and competitive fitness in primary human airway epithelial c
52 c Escherichia coli (EHEC), required for full competitive fitness in the mouse gut and highly expresse
53 g these compensatory mutations showed a high competitive fitness in vitro.
54 enhanced proliferation, and profound loss of competitive fitness in vivo.
55 ion for specific mutations that increase HSC competitive fitness, in conjunction with additional endo
56 ions in the assay experiment, from which new competitive fitness indices or parameters are defined.
57 s is 0.17%/generation; that of hermaphrodite competitive fitness is 0.11%/generation.
58         The rate of mutational decay of male competitive fitness is 0.17%/generation; that of hermaph
59 rent from zero, whereas VM for hermaphrodite competitive fitness is similar to that of non-competitiv
60 ext of the pulmonary microbiome, interstrain competitive fitness may be another factor that influence
61        BCR(-) lymphoma variants that restore competitive fitness normalize GSK3beta activity after co
62 tance plasmids and measured their effects on competitive fitness of a Pseudomonas fluorescens SBW25 h
63 -1 rejuvenates aged niche cells and restores competitive fitness of aged blood stem cells to youthful
64 ing these systems may also contribute to the competitive fitness of B. pseudomallei.
65 immune selection against hyphae improves the competitive fitness of C. albicans.
66 ugh a noncanonical pathway, IL-6 can improve competitive fitness of CD4 T cells by facilitating cell
67 ects were most apparent as a decrease in the competitive fitness of cells lacking 6S RNA.
68 involved in L-serine utilization reduces the competitive fitness of E. coli LF82 and Citrobacter rode
69 th virulence regulation in order to maximise competitive fitness of enteric pathogens within the host
70 roducible, systematic assay to determine the competitive fitness of HIV-1 drug-resistant mutants.
71 d due to nonlethal mutations, we measure the competitive fitness of hundreds of randomly selected clo
72     Despite evidence that KLRG1 impaired the competitive fitness of lung ILC2s during inflammation, K
73 exhibited normal thymic Treg generation, the competitive fitness of peripheral Tregs was severely com
74 iabetes or diet-induced obesity enhanced the competitive fitness of Pik3ca(H1047R) cells.
75                         Mechanistically, the competitive fitness of S. aureus is a result of both agr
76 romote clonal hematopoiesis by improving the competitive fitness of specific hematopoietic stem cell
77 required for maintaining the homeostasis and competitive fitness of T(reg) cells in vivo.
78 enhance acid tolerance and contribute to the competitive fitness of the organism at low pH.
79 xp3-dependent regulation of miR155 maintains competitive fitness of Treg cell subsets by targeting SO
80 odel approach for more-accurate estimates of competitive fitness parameters from multiple data points
81 dentified, mechanisms that help maintain the competitive fitness potential of nondividing bacterial p
82 undergo regulated cell death to maintain the competitive fitness potential of the population.
83                                 However, low competitive fitness, pre-immune humans and the benefit o
84 survival of early neoplasms depends on their competitive fitness relative to that of mutant clones in
85                                 By examining competitive fitness relative to that of ZIKV M1404, we o
86                                            A competitive fitness study failed to reveal any differenc
87 elates with the width of the distribution of competitive fitness, such that physical environments wit
88 le number have a quadratic relationship with competitive fitness, suggesting stabilizing selection fo
89                                              Competitive fitness tests in generations 50 and 85 showe
90 significantly faster and displayed increased competitive fitness than the wild-type virus in hamsters
91  over the population had significantly lower competitive fitness than two clones with mutations that
92        Wild-type nematodes exhibited greater competitive fitness than unc-22(sf21) mutants.
93  mutagenesis coupled with direct measures of competitive fitness to estimate the distribution of fitn
94 nmental Aux3 acquisition conferred increased competitive fitness to pre-pandemic V. cholerae, leading
95  spread of low-resistance variants with high competitive fitness under these conditions.
96                                              Competitive fitness, viability and fertility of the chro
97 mal locus required for copper resistance and competitive fitness was cloned from a strain of Pseudomo
98 ctivation in TAMs and cancer cells and their competitive fitness were dependent on the endolysosomal
99 dent Rbs(-) mutants were isolated, and their competitive fitnesses were measured relative to that of
100 n in the intestine, suggesting they may lose competitive fitness when grown outside the gut.
101 at deletion of type IV SCCmec did not affect competitive fitness, whereas deletion of ACME significan
102 ation, stress response, and adhesion to gain competitive fitness, while previous exposure to antibiot
103 MHV-ExoN-AA showed increased replication and competitive fitness without reversion of ExoN-AA.

 
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