MOESM4 of Identification of drought stress related proteins from 1Sl(1B) chromosome substitution line of wheat variety Chinese Spring

Additional file 4: Figure S3. Proteome maps of wheat albumins and globulins from mature grains of CS and CS-1Sl (1B). S1 to S25 represented those specifically expressed in CS-1Sl (1B). The detail identification results were showed in Table1

MOESM3 of Identification of drought stress related proteins from 1Sl(1B) chromosome substitution line of wheat variety Chinese Spring

Additional file 3: Figure S2. Pictures of CS-1Sl (1B) under drought stress and well-watered conditions in several grains development stages. (a).After tillering; (b). After harvest; (c). 5DPA; (d). 30 DPA

MOESM2 of Identification of drought stress related proteins from 1Sl(1B) chromosome substitution line of wheat variety Chinese Spring

Additional file 2: Table S1. Some agronomic character performance of CS-1Sl (1B) under drought stress and well-watered conditions

MOESM5 of Identification of drought stress related proteins from 1Sl(1B) chromosome substitution line of wheat variety Chinese Spring

Additional file 5: Table S2. Peptide sequences of mature seed proteins encoded by 1Sl genome of CS-1Sl(1B) identified by MALDI-TOF/TOF-MS

MOESM1 of Identification of drought stress related proteins from 1Sl(1B) chromosome substitution line of wheat variety Chinese Spring

Additional file 1: Figure S1. Performance of drought tolerance between CS and CS-1Sl (1B)

Image_2_JIP1 Deficiency Protects Retinal Ganglion Cells From Apoptosis in a Rotenone-Induced Injury Model.TIF

Retinal ganglion cells (RGCs) undergo apoptosis after injury. c-Jun N-terminal kinase (JNK)-interacting protein 1 (JIP1) is a scaffold protein that is relevant to JNK activation and a key molecule known to regulate neuronal apoptosis. However, the specific role of JIP1 in the apoptosis of RGCs is currently undefined. Here, we used JIP1 gene knockout (KO) mice to investigate the importance of JIP1-JNK signaling in the apoptosis of RGCs in a rotenone-induced injury model. In adult JIP1 KO mice, the number and electrophysiological functions of RGCs were not different from those of wild-type (WT) mice. Ablation of JIP1 attenuated the activation of JNK and the cleavage of caspase-3 in the retina after rotenone injury and contributed to a lower number of TUNEL-positive RGCs, a greater percentage of surviving RGCs, and a significant reduction in the electrophysiological functional loss of RGCs when compared to those in WT controls. We also found that JIP1 was located in the neurites of primary RGCs, but accumulated in soma in response to rotenone treatment. Moreover, the number of TUNEL-positive RGCs, the level of activation of JNK and the rate of cleavage of caspase-3 were reduced in primary JIP1-deficient RGCs after rotenone injury than in WT controls. Together, our results demonstrate that the JIP1-mediated activation of JNK contributes to the apoptosis of RGCs in a rotenone-induced injury model in vitro and in vivo, suggesting that JIP1 may be a potential therapeutic target for RGC degeneration.</p

Image_1_JIP1 Deficiency Protects Retinal Ganglion Cells From Apoptosis in a Rotenone-Induced Injury Model.TIF

Retinal ganglion cells (RGCs) undergo apoptosis after injury. c-Jun N-terminal kinase (JNK)-interacting protein 1 (JIP1) is a scaffold protein that is relevant to JNK activation and a key molecule known to regulate neuronal apoptosis. However, the specific role of JIP1 in the apoptosis of RGCs is currently undefined. Here, we used JIP1 gene knockout (KO) mice to investigate the importance of JIP1-JNK signaling in the apoptosis of RGCs in a rotenone-induced injury model. In adult JIP1 KO mice, the number and electrophysiological functions of RGCs were not different from those of wild-type (WT) mice. Ablation of JIP1 attenuated the activation of JNK and the cleavage of caspase-3 in the retina after rotenone injury and contributed to a lower number of TUNEL-positive RGCs, a greater percentage of surviving RGCs, and a significant reduction in the electrophysiological functional loss of RGCs when compared to those in WT controls. We also found that JIP1 was located in the neurites of primary RGCs, but accumulated in soma in response to rotenone treatment. Moreover, the number of TUNEL-positive RGCs, the level of activation of JNK and the rate of cleavage of caspase-3 were reduced in primary JIP1-deficient RGCs after rotenone injury than in WT controls. Together, our results demonstrate that the JIP1-mediated activation of JNK contributes to the apoptosis of RGCs in a rotenone-induced injury model in vitro and in vivo, suggesting that JIP1 may be a potential therapeutic target for RGC degeneration.</p

Image_3_JIP1 Deficiency Protects Retinal Ganglion Cells From Apoptosis in a Rotenone-Induced Injury Model.TIF

Retinal ganglion cells (RGCs) undergo apoptosis after injury. c-Jun N-terminal kinase (JNK)-interacting protein 1 (JIP1) is a scaffold protein that is relevant to JNK activation and a key molecule known to regulate neuronal apoptosis. However, the specific role of JIP1 in the apoptosis of RGCs is currently undefined. Here, we used JIP1 gene knockout (KO) mice to investigate the importance of JIP1-JNK signaling in the apoptosis of RGCs in a rotenone-induced injury model. In adult JIP1 KO mice, the number and electrophysiological functions of RGCs were not different from those of wild-type (WT) mice. Ablation of JIP1 attenuated the activation of JNK and the cleavage of caspase-3 in the retina after rotenone injury and contributed to a lower number of TUNEL-positive RGCs, a greater percentage of surviving RGCs, and a significant reduction in the electrophysiological functional loss of RGCs when compared to those in WT controls. We also found that JIP1 was located in the neurites of primary RGCs, but accumulated in soma in response to rotenone treatment. Moreover, the number of TUNEL-positive RGCs, the level of activation of JNK and the rate of cleavage of caspase-3 were reduced in primary JIP1-deficient RGCs after rotenone injury than in WT controls. Together, our results demonstrate that the JIP1-mediated activation of JNK contributes to the apoptosis of RGCs in a rotenone-induced injury model in vitro and in vivo, suggesting that JIP1 may be a potential therapeutic target for RGC degeneration.</p