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All of the mutants lacking a single gerP gene (or lacking the three gerPF family members) also exhibited this germination defect when compared to wild-type (Table 5).
The defect model adopted in this study exhibited buccal open defect and lingual coronal defect areas around the upper 3 mm portion of implants.
Experiments using TLR2, 3, 4, 7 gene-deficient mice exhibited no defects in this response whereas a reduction was observed in MyD88 knock-out mice.
This mutant strain exhibited a growth defect, was resistant to amphotericin B, and was hypersensitive to other sterol inhibitors.
The ΔgerP-null strain, however, exhibited a germination defect in this solution with only a 30% loss of heat resistant spores after 30 minutes (Figure 5).
This mutant also exhibited multiple defects in hyphal growth and asexual sporulation (Table 1 and Table 3).
These mutant mice exhibited a neurological defect.
The OsIRE1 knockdown (KD) lines exhibited severe defects in growth and so were difficult to maintain.
Previously reported Mib1−/− mice exhibited multiple defects in neurogenesis, somitogenesis, vasculogenesis, and cardiogenesis [13].
The animals exhibited morphological defects in the Malpighian tubules and underwent complete developmental arrest as prepupae.
Moreover, we found that univalents exhibited congression defects on bipolar spindles.
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