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However, only weak GUS staining was observed in the scutella of embryos of mature seeds, although no staining was found in endosperms (T3, Figure 4G).
In addition, transgenic plants #2 and #7 of Oshsp17.3Pro-ΔAZRE::GUS (Oshsp17.3pΔAZRE), which showed weak GUS expression with HS and AZC treatment (Guan et al. 2010), were used as the negative control.
When the LRP developed to a hemispherical shape, a weak GUS activity was detected in the center of LRP, indicating a weak expression of OsPIN1b at this stage (Figure 3D2).
Weak GUS staining was detected in root hairs (Figure 7E) and all cell layers of the root tip (Figure 7F).
In the petiole only very weak GUS expression was present.
There was also weak GUS activity in the upper part of the pistil.
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In light of the molecular lesion found in CS3227, we re-examined the circadian defects present in CS3227 alongside the weak gi allele gi-1 and the strong alleles gi-2 and gi-201.
Conversely, weaker GUS staining was observed in the mature pollen in all transgenic lines when the GUS reporter gene was driven by the AtPTPC gene promoters (ProAtppc1- 3).
Chemical staining also showed that the pBI121m seedlings displayed weaker GUS activities than the pBI121 seedlings (Fig. 8c).
The expression activity of GmPRP2p-471 was extremely weak, and GUS staining was not detectable by eyes.
When compared with the 1651-pBI lines, very weak and weak/moderate GUS intensity was present in the 256-pBI and 284-pBI lines, respectively (Additional file 2: Table S1).
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