This is the actal papers link: https://academic.oup.com/hmg/article/23/1/69/7221
ID: 151016 • Letter: T
Question
This is the actal papers link: https://academic.oup.com/hmg/article/23/1/69/722169
and these are the graphs I need to be able to explain:
Figure 5
The caption below is this:
Reduction of Cdk5 activity does not improve subsynaptic DNA damage in mSCS muscle. (A) Upper: immunostaining of Cdk5 (green) co-localized with NMJ (red) in WT and mSCS. No morphological changes were identified between WT, mSCS and treated mSCS TA muscle. Middle: Cdk5 activity is increased in mSCS muscle compared with WT. Electroporation of Cdk5DN plasmid reduced Cdk5-dependent phosphorylated Histone H1 level in mSCS muscle, whereas API4 expression had no effect on Cdk5 activity. Lower: quantification of Cdk5 activity in WT, mSCS and treated mSCS TA muscle expressed as the ratio of phosphorylated histone H1 level to Cdk5 protein expression level (# = normalized to WT). In mSCS-Cdk5DN, Cdk5 activity was 0.63 ± 0.13 of WT, compared with 2.2 ± 0.3 in SCS, 2.2 ± 0.1 in mSCS-API4 and 2.2 ± 0.2 in mSCS-pcDNA3. n = 3; *P < 0.05, Mann–Whitney U-test. (B) Quantitation of p-H2AX-labeled endplates in WT, mSCS and treated mSCS. p-H2AX-labeled endplates in mSCS-Cdk5DN was 35.7 ± 2.0%, compared with 37.3 ± 2.2% in mSCS and 35.6 ± 3.3% in mSCS control (mSCS-pcDNA3). n = 5; P > 0.98. p-H2AX-labeled endplates in WT was 1.42 ± 1.23%. n = 5; ***P < 0.001, Student's t-test. To investigate the role of dys The caption below is this:
Reduction of Cdk5 activity does not improve subsynaptic DNA damage in mSCS muscle. (A) Upper: immunostaining of Cdk5 (green) co-localized with NMJ (red) in WT and mSCS. No morphological changes were identified between WT, mSCS and treated mSCS TA muscle. Middle: Cdk5 activity is increased in mSCS muscle compared with WT. Electroporation of Cdk5DN plasmid reduced Cdk5-dependent phosphorylated Histone H1 level in mSCS muscle, whereas API4 expression had no effect on Cdk5 activity. Lower: quantification of Cdk5 activity in WT, mSCS and treated mSCS TA muscle expressed as the ratio of phosphorylated histone H1 level to Cdk5 protein expression level (# = normalized to WT). In mSCS-Cdk5DN, Cdk5 activity was 0.63 ± 0.13 of WT, compared with 2.2 ± 0.3 in SCS, 2.2 ± 0.1 in mSCS-API4 and 2.2 ± 0.2 in mSCS-pcDNA3. n = 3; *P < 0.05, Mann–Whitney U-test. (B) Quantitation of p-H2AX-labeled endplates in WT, mSCS and treated mSCS. p-H2AX-labeled endplates in mSCS-Cdk5DN was 35.7 ± 2.0%, compared with 37.3 ± 2.2% in mSCS and 35.6 ± 3.3% in mSCS control (mSCS-pcDNA3). n = 5; P > 0.98. p-H2AX-labeled endplates in WT was 1.42 ± 1.23%. n = 5; ***P < 0.001, Student's t-test. To investigate the role of dys Reduction of Cdk5 activity does not improve subsynaptic DNA damage in mSCS muscle. (A) Upper: immunostaining of Cdk5 (green) co-localized with NMJ (red) in WT and mSCS. No morphological changes were identified between WT, mSCS and treated mSCS TA muscle. Middle: Cdk5 activity is increased in mSCS muscle compared with WT. Electroporation of Cdk5DN plasmid reduced Cdk5-dependent phosphorylated Histone H1 level in mSCS muscle, whereas API4 expression had no effect on Cdk5 activity. Lower: quantification of Cdk5 activity in WT, mSCS and treated mSCS TA muscle expressed as the ratio of phosphorylated histone H1 level to Cdk5 protein expression level (# = normalized to WT). In mSCS-Cdk5DN, Cdk5 activity was 0.63 ± 0.13 of WT, compared with 2.2 ± 0.3 in SCS, 2.2 ± 0.1 in mSCS-API4 and 2.2 ± 0.2 in mSCS-pcDNA3. n = 3; *P < 0.05, Mann–Whitney U-test. (B) Quantitation of p-H2AX-labeled endplates in WT, mSCS and treated mSCS. p-H2AX-labeled endplates in mSCS-Cdk5DN was 35.7 ± 2.0%, compared with 37.3 ± 2.2% in mSCS and 35.6 ± 3.3% in mSCS control (mSCS-pcDNA3). n = 5; P > 0.98. p-H2AX-labeled endplates in WT was 1.42 ± 1.23%. n = 5; ***P < 0.001, Student's t-test. To investigate the role of dys Reduction of Cdk5 activity does not improve subsynaptic DNA damage in mSCS muscle. (A) Upper: immunostaining of Cdk5 (green) co-localized with NMJ (red) in WT and mSCS. No morphological changes were identified between WT, mSCS and treated mSCS TA muscle. Middle: Cdk5 activity is increased in mSCS muscle compared with WT. Electroporation of Cdk5DN plasmid reduced Cdk5-dependent phosphorylated Histone H1 level in mSCS muscle, whereas API4 expression had no effect on Cdk5 activity. Lower: quantification of Cdk5 activity in WT, mSCS and treated mSCS TA muscle expressed as the ratio of phosphorylated histone H1 level to Cdk5 protein expression level (# = normalized to WT). In mSCS-Cdk5DN, Cdk5 activity was 0.63 ± 0.13 of WT, compared with 2.2 ± 0.3 in SCS, 2.2 ± 0.1 in mSCS-API4 and 2.2 ± 0.2 in mSCS-pcDNA3. n = 3; *P < 0.05, Mann–Whitney U-test. (B) Quantitation of p-H2AX-labeled endplates in WT, mSCS and treated mSCS. p-H2AX-labeled endplates in mSCS-Cdk5DN was 35.7 ± 2.0%, compared with 37.3 ± 2.2% in mSCS and 35.6 ± 3.3% in mSCS control (mSCS-pcDNA3). n = 5; P > 0.98. p-H2AX-labeled endplates in WT was 1.42 ± 1.23%. n = 5; ***P < 0.001, Student's t-test. To investigate the role of dys Cdk5/AChR/DAPI WT mSCS mSCS- mSCS- mSCS- WT Cdk5DN mSCS pcDNA3 API4 3 CO 0 WT m SCS mSCS mSCS- mSCS- pcDNA3 API4 Cdk5DN 50 40 30 20 5 10 mSCS mSCS- mSCS- pcDNA3 Cdk5DN
Explanation / Answer
The explanation can be found as below:
According to the graphical and illustrative representation, it can be seen that in vitro fluorescent imaging as well as electrophoresis followed by western blotting has been performed in these investigations. The observance of western blots was quantized by translating the band density using online available software and a graphical representation was produced in the form of a bar graph. Different representations of the results was performed.
In order to understand and interpret the electrophoretic data, one should look at the band density or at the graphical representation directly. More is the signal intensity, more is the expression of the protein being investigated. Hence, it can be stated from the information that the expression of phsohporylated histone H1 is maximum in mSCS cells. Further, the expression of cdk5 was also performed and it was found that three experimental groups were showing maximum activity. Together from these two graphs, it can be concluded that the mSCS cells showed maximum cdk5 activity due to loosening of the chromatin secondary to phosphorylation of histone H1, thereby increasing the transcription of genes related for this activity.
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