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Editor’s note iNature is China’s largest academic official account.
It is jointly created by the doctoral team of Tsinghua University, Harvard University, Chinese Academy of Sciences and other units.
The iNature Talent Official Account is now launched, focusing on talent recruitment, academic progress, scientific research information, interested parties can Long press or scan the QR code below to follow us
.
iNatureSUMOylation is similar to ubiquitination.
It is an important type of protein post-translational modification in eukaryotes, regulating transcription factor activation, epigenetic regulation, DNA damage repair and other biological processes
.
SENP2 (Sentrin/SUMO-specific proteases, SENPs), as an important class of de-SUMO-modifying enzymes, is essential to maintain the homeostasis of SUMO modification in eukaryotic cells, and is further involved in the regulation of important life activities such as embryonic development and heart formation.
Closely related, but the regulation mechanism of SENP2 in neurogenesis is still unknown
.
On August 31, 2021, Qi Yitao, Wu Hongmei of the School of Life Sciences of Shaanxi Normal University and Edward Yeh of the University of Arkansas jointly published an online report entitled "SENP2-PLCβ4 signaling regulates neurogenesis through the" in Cell Death and Differentiation (IF=15.
83).
maintenance of calcium homeostasis" research paper
.
The study found that SENP2 not only has an important regulatory effect on mouse embryonic development and neuronal electrophysiological functions, but also maintains the steady state of the number of mouse hippocampal neurons, and regulates the calcium of adult mouse neurons through the SENP2-PLCβ4 signal axis.
Homeostasis, which in turn regulates the neurogenesis process in the granular area of the hippocampal dentate gyrus
.
In summary, this study reveals the key role of SENP2 protein in regulating the deSUMO modification of PLCβ4 protein, and confirms that the SENP2-PLCβ4 axis plays an important role in regulating neurogenesis through calcium homeostasis, and is important for maintaining the homeostasis of neural stem cell self-renewal.
Meaning
.
Neurogenesis refers to the process of generating new functional neurons in a specific area of the nervous system.
Adult neurogenesis plays a key role in brain damage repair, maintenance of smell, and behavioral performance.
It is also an important factor in the maintenance of learning and memory functions in the hippocampus.
One
.
Calcium homeostasis is an important basis for maintaining the normal physiological functions of the nervous system.
The imbalance of neuronal calcium homeostasis can lead to disorders of various cellular physiological processes, causing neuronal differentiation disorders, neurodevelopmental defects, and neurodegenerative diseases And many other diseases occur
.
Phospholipase C subtype β4 (PLCβ4), as an important type of phospholipase in the central nervous system, precisely regulates the inositol metabolism of neurons, thereby affecting key calcium channels in the endoplasmic reticulum, regulating cytoplasmic calcium homeostasis, and affecting downstream Signal transmission, but there is no report on the regulation of PLCβ4 on neurogenesis
.
SENP2, as an important SUMO-specific protease, is essential to maintain the homeostasis of SUMO modification in eukaryotic cells, and is closely related to the occurrence and development of many human diseases
.
Previous studies have found that SENP2 can affect and regulate the function of the central nervous system, causing sudden epileptic death in mice
.
In-depth exploration of the important role and molecular mechanism of SENP2 regulation of SUMO modification in the maintenance of neuronal function and neurogenesis will provide a new biological basis for SUMO modification to regulate neurogenesis, and provide a new role for clinical treatment of neurogenesis disorders Target and theoretical basis
.
The study first conducted a neurobiological correlation analysis on the granular area of the hippocampal dentate gyrus of SENP2-deficient mice, and found that the number of neurons in the granular area of the hippocampus dentate gyrus of SENP2-deficient mice was before sudden epilepsy death (4-6 Week-old) significant loss occurs, accompanied by obvious glial activation
.
Subsequently, the study conducted an in-depth analysis of the hippocampal neuron types of SENP2-deficient mice, combined with the proliferation of neural stem cells in vivo, and confirmed that SENP2 deficiency can lead to imbalance of neuronal calcium homeostasis and affect the self-renewal of neural stem cells, which further causes adult mice’s dysfunction.
Neurogenesis is blocked
.
The study also conducted an in-depth exploration of the molecular mechanisms behind the phenotype
.
First, the study found that SENP2 can regulate the SUMO modification of PLCβ4, a key protein for calcium homeostasis maintenance, and affect its protein expression from the post-translational modification level; second, the research team used protein degradation experiments to clarify that SENP2 regulates the SUMO modification of PLCβ4 This in turn affects the ubiquitination and degradation of its protein; at the same time, through subcellular localization analysis and cell nucleoplasmic protein component separation experiments, it is determined that SUMO modification can also regulate the subcellular localization of PLCβ4 protein; finally, the use of co-immunoprecipitation combined with mass spectrometry Data analysis of the regulatory mechanism of SUMO modification regulating the nucleocytoplasmic shuttle of PLCβ4 protein confirms the key regulatory effect of SENP2 on PLCβ4 from the molecular level
.
In summary, this study reveals the role of SUMO modification of PLCβ4 on the regulation of calcium homeostasis and neurogenesis from the perspective of oxidative stress
.
PLCβ4 in the hippocampus of SENP2-deficient mice is over-SUMO-modified, breaking its own subcellular localization, promoting its nuclear transport and activating the subsequent ubiquitination degradation pathway
.
The imbalance of PLCβ4 protein homeostasis will further induce the damage of intracellular calcium homeostasis and eventually lead to neurogenesis in adult mice
.
This study provides a new exploration perspective for the regulation mode of GPCR signaling pathway from the level of protein post-translational modification
.
It shows that balancing the SENP2-PLCβ4 signal axis will become a new intervention for neurological diseases caused by adult neurogenesis defects (Figure 1)
.
Figure 1.
The model of the SENP2-PLCβ4 signal axis regulating adult mouse neurogenesis.
Chen Xu, a doctoral student in the School of Life Sciences, Shaanxi Normal University, is the first author.
Professor Qi Yitao, Associate Professor Wu Hongmei and Professor Edward Yeh of the University of Arkansas are the co-corresponding authors
.
The research was also greatly assisted by Professor Cheng Jinke from Shanghai Jiaotong University School of Medicine
.
At the same time, Professor Li Xing and Professor Tian Yingfang from the School of Life Sciences of Shaanxi Normal University also provided strong support
.
Reference message: https://
It is jointly created by the doctoral team of Tsinghua University, Harvard University, Chinese Academy of Sciences and other units.
The iNature Talent Official Account is now launched, focusing on talent recruitment, academic progress, scientific research information, interested parties can Long press or scan the QR code below to follow us
.
iNatureSUMOylation is similar to ubiquitination.
It is an important type of protein post-translational modification in eukaryotes, regulating transcription factor activation, epigenetic regulation, DNA damage repair and other biological processes
.
SENP2 (Sentrin/SUMO-specific proteases, SENPs), as an important class of de-SUMO-modifying enzymes, is essential to maintain the homeostasis of SUMO modification in eukaryotic cells, and is further involved in the regulation of important life activities such as embryonic development and heart formation.
Closely related, but the regulation mechanism of SENP2 in neurogenesis is still unknown
.
On August 31, 2021, Qi Yitao, Wu Hongmei of the School of Life Sciences of Shaanxi Normal University and Edward Yeh of the University of Arkansas jointly published an online report entitled "SENP2-PLCβ4 signaling regulates neurogenesis through the" in Cell Death and Differentiation (IF=15.
83).
maintenance of calcium homeostasis" research paper
.
The study found that SENP2 not only has an important regulatory effect on mouse embryonic development and neuronal electrophysiological functions, but also maintains the steady state of the number of mouse hippocampal neurons, and regulates the calcium of adult mouse neurons through the SENP2-PLCβ4 signal axis.
Homeostasis, which in turn regulates the neurogenesis process in the granular area of the hippocampal dentate gyrus
.
In summary, this study reveals the key role of SENP2 protein in regulating the deSUMO modification of PLCβ4 protein, and confirms that the SENP2-PLCβ4 axis plays an important role in regulating neurogenesis through calcium homeostasis, and is important for maintaining the homeostasis of neural stem cell self-renewal.
Meaning
.
Neurogenesis refers to the process of generating new functional neurons in a specific area of the nervous system.
Adult neurogenesis plays a key role in brain damage repair, maintenance of smell, and behavioral performance.
It is also an important factor in the maintenance of learning and memory functions in the hippocampus.
One
.
Calcium homeostasis is an important basis for maintaining the normal physiological functions of the nervous system.
The imbalance of neuronal calcium homeostasis can lead to disorders of various cellular physiological processes, causing neuronal differentiation disorders, neurodevelopmental defects, and neurodegenerative diseases And many other diseases occur
.
Phospholipase C subtype β4 (PLCβ4), as an important type of phospholipase in the central nervous system, precisely regulates the inositol metabolism of neurons, thereby affecting key calcium channels in the endoplasmic reticulum, regulating cytoplasmic calcium homeostasis, and affecting downstream Signal transmission, but there is no report on the regulation of PLCβ4 on neurogenesis
.
SENP2, as an important SUMO-specific protease, is essential to maintain the homeostasis of SUMO modification in eukaryotic cells, and is closely related to the occurrence and development of many human diseases
.
Previous studies have found that SENP2 can affect and regulate the function of the central nervous system, causing sudden epileptic death in mice
.
In-depth exploration of the important role and molecular mechanism of SENP2 regulation of SUMO modification in the maintenance of neuronal function and neurogenesis will provide a new biological basis for SUMO modification to regulate neurogenesis, and provide a new role for clinical treatment of neurogenesis disorders Target and theoretical basis
.
The study first conducted a neurobiological correlation analysis on the granular area of the hippocampal dentate gyrus of SENP2-deficient mice, and found that the number of neurons in the granular area of the hippocampus dentate gyrus of SENP2-deficient mice was before sudden epilepsy death (4-6 Week-old) significant loss occurs, accompanied by obvious glial activation
.
Subsequently, the study conducted an in-depth analysis of the hippocampal neuron types of SENP2-deficient mice, combined with the proliferation of neural stem cells in vivo, and confirmed that SENP2 deficiency can lead to imbalance of neuronal calcium homeostasis and affect the self-renewal of neural stem cells, which further causes adult mice’s dysfunction.
Neurogenesis is blocked
.
The study also conducted an in-depth exploration of the molecular mechanisms behind the phenotype
.
First, the study found that SENP2 can regulate the SUMO modification of PLCβ4, a key protein for calcium homeostasis maintenance, and affect its protein expression from the post-translational modification level; second, the research team used protein degradation experiments to clarify that SENP2 regulates the SUMO modification of PLCβ4 This in turn affects the ubiquitination and degradation of its protein; at the same time, through subcellular localization analysis and cell nucleoplasmic protein component separation experiments, it is determined that SUMO modification can also regulate the subcellular localization of PLCβ4 protein; finally, the use of co-immunoprecipitation combined with mass spectrometry Data analysis of the regulatory mechanism of SUMO modification regulating the nucleocytoplasmic shuttle of PLCβ4 protein confirms the key regulatory effect of SENP2 on PLCβ4 from the molecular level
.
In summary, this study reveals the role of SUMO modification of PLCβ4 on the regulation of calcium homeostasis and neurogenesis from the perspective of oxidative stress
.
PLCβ4 in the hippocampus of SENP2-deficient mice is over-SUMO-modified, breaking its own subcellular localization, promoting its nuclear transport and activating the subsequent ubiquitination degradation pathway
.
The imbalance of PLCβ4 protein homeostasis will further induce the damage of intracellular calcium homeostasis and eventually lead to neurogenesis in adult mice
.
This study provides a new exploration perspective for the regulation mode of GPCR signaling pathway from the level of protein post-translational modification
.
It shows that balancing the SENP2-PLCβ4 signal axis will become a new intervention for neurological diseases caused by adult neurogenesis defects (Figure 1)
.
Figure 1.
The model of the SENP2-PLCβ4 signal axis regulating adult mouse neurogenesis.
Chen Xu, a doctoral student in the School of Life Sciences, Shaanxi Normal University, is the first author.
Professor Qi Yitao, Associate Professor Wu Hongmei and Professor Edward Yeh of the University of Arkansas are the co-corresponding authors
.
The research was also greatly assisted by Professor Cheng Jinke from Shanghai Jiaotong University School of Medicine
.
At the same time, Professor Li Xing and Professor Tian Yingfang from the School of Life Sciences of Shaanxi Normal University also provided strong support
.
Reference message: https://
