cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.7608515.v1
title: Additional file 1: of Integrated physiological and proteomic analysis of embryo and endosperm reveals central salt stress response proteins during seed germination of winter wheat cultivar Zhengmai 366

description: Table S1–1. DAPs from embryo samples identified by MALDI-TOF/TOF-MS under salt stress. Table S1–2. DAPs from endosperm samples identified by MALDI-TOF/TOF-MS under salt stress. Table S2–1. The peptide information of all the identified proteins in the embryo under salt stress. Table S2–2. The peptide information of all the identified proteins in the endosperm under salt stress. (XLSX 161 kb)
DOI: 10.6084/m9.figshare.7608521
title: Additional file 2: of Integrated physiological and proteomic analysis of embryo and endosperm reveals central salt stress response proteins during seed germination of winter wheat cultivar Zhengmai 366

description: Table S3. Gene-specific primers sequences for subcellular localization. (XLSX 9 kb)
DOI: 10.6084/m9.figshare.7608521.v1
title: Additional file 2: of Integrated physiological and proteomic analysis of embryo and endosperm reveals central salt stress response proteins during seed germination of winter wheat cultivar Zhengmai 366

description: Table S3. Gene-specific primers sequences for subcellular localization. (XLSX 9 kb)
DOI: 10.5281/zenodo.10658793
title: How to Make Antibodies in Bacillus subtilis - Supplemental Data
DOI: 10.5281/zenodo.10658794
title: How to Make Antibodies in Bacillus subtilis - Supplemental Data
DOI: 10.5281/zenodo.10664122
title: How to Make Antibodies in Bacillus subtilis - Supplemental Data
DOI: 10.6084/m9.figshare.12851402.v2
title: The Unfolded Protein Response Regulates Hepatic Autophagy by sXBP1-mediated Activation of TFEB

description: Defective macroautophagy/autophagy and a failure to initiate the adaptive unfolded protein response (UPR) in response to the endoplasmic reticulum (ER) stress contributes to obesity-associated metabolic dysfunction. However, whether and how unresolved ER stress leads to defects in the autophagy pathway and to the progression of obesity-associated hepatic pathologies remains unclear. Obesity suppresses the expression of hepatic spliced XBP1 (X-box binding protein 1; sXBP1), the key transcription factor that promotes the adaptive UPR. Our RNA-seq analysis revealed that sXBP1 regulates genes involved in lysosomal function in the liver under fasting conditions. Chromatin immunoprecipitation (ChIP) analyses of both primary hepatocytes and whole liver further showed that sXBP1 occupies the -743 to -523 site of the promoter of <i>Tfeb</i> (transcription factor EB), a master regulator of autophagy and lysosome biogenesis. Notably, this occupancy was significantly reduced in livers from patients with steatosis. In mice, hepatic deletion of <i>Xbp1</i> (<i>xbp1</i> LKO) suppressed the transcription of <i>Tfeb</i> as well as autophagy, whereas hepatic overexpression of s<i>Xbp1</i> enhanced <i>Tfeb</i> transcription and autophagy. Moreover, overexpression of <i>Tfeb</i> in the <i>xbp1</i> LKO mouse liver ameliorated glucose intolerance and steatosis in mice with diet-induced obesity (DIO). Conversely, loss of TFEB function impaired the protective role of sXBP1 in hepatic steatosis in mice with DIO. These data indicate that sXBP1-<i>Tfeb</i> signaling has direct functional consequences in the context of obesity. Collectively, our data provide novel insight into how two organelle stress responses are integrated to protect against obesity-associated metabolic dysfunction.
DOI: 10.6084/m9.figshare.12851405
title: Autophagy core protein ATG5 is required for elongating spermatid development, sperm individualization and normal fertility in male mice

description: Spermiogenesis is the longest phase of spermatogenesis, with dramatic morphological changes and a final step of spermiation, which involves protein degradation and the removal of excess cytoplasm; therefore, we hypothesized that macroautophagy/autophagy might be involved in the process. To test this hypothesis, we examined the function of ATG5, a core autophagy protein in male germ cell development. Floxed <i>Atg5</i> and <i>Stra8− iCre</i> mice were crossed to conditionally inactivate <i>Atg5</i> in male germ cells. In <i>Atg5<sup>flox/flox</sup>; Stra8− iCre</i> mutant mice, testicular expression of the autophagosome marker LC3A/B-II was significantly reduced, and expression of autophagy receptor SQSTM1/p62 was significantly increased, indicating a decrease in testicular autophagy activity. The fertility of mutant mice was dramatically reduced with about 70% being infertile. Sperm counts and motility were also significantly reduced compared to controls. Histological examination of the mutant testes revealed numerous, large residual bodies in the lumen of stages after their normal resorption within the seminiferous epithelium. The cauda epididymal lumen was filled with sloughed germ cells, large cytoplasmic bodies, and spermatozoa with disorganized heads and tails. Examination of cauda epididymal sperm by electron microscopy revealed misshapen sperm heads, a discontinuous accessory structure in the mid-piece and abnormal acrosome formation and loss of sperm individualization. Immunofluorescence staining of epididymal sperm showed abnormal mitochondria and acrosome distribution in the mutant mice. ATG5 was shown to induce autophagy by mediating multiple signals to maintain normal developmental processes. Our study demonstrated ATG5 is essential for male fertility and is involved in various aspects of spermiogenesis. <b>Abbreviations</b>: AKAP4: a-kinase anchoring protein 4; ATG5: autophagy-related 5; ATG7: autophagy-related 7; ATG10: autophagy-related 10; ATG12: autophagy-related 12; cKO: conditional knockout; DDX4: DEAD-box helicase 4; MAP1LC3/LC3/tg8: microtubule-associated protein 1 light chain 3; PBS: phosphate-buffered saline; PIWIL2/MILI: piwi like RNA-mediated gene silencing 2; RT-PCR: reverse transcription-polymerase chain reaction; SQSTM1/p62: sequestosome 1; TBC: tubulobulbar complexes; WT: wild type.
DOI: 10.6084/m9.figshare.12851405.v1
title: Autophagy core protein ATG5 is required for elongating spermatid development, sperm individualization and normal fertility in male mice

description: Spermiogenesis is the longest phase of spermatogenesis, with dramatic morphological changes and a final step of spermiation, which involves protein degradation and the removal of excess cytoplasm; therefore, we hypothesized that macroautophagy/autophagy might be involved in the process. To test this hypothesis, we examined the function of ATG5, a core autophagy protein in male germ cell development. Floxed <i>Atg5</i> and <i>Stra8− iCre</i> mice were crossed to conditionally inactivate <i>Atg5</i> in male germ cells. In <i>Atg5<sup>flox/flox</sup>; Stra8− iCre</i> mutant mice, testicular expression of the autophagosome marker LC3A/B-II was significantly reduced, and expression of autophagy receptor SQSTM1/p62 was significantly increased, indicating a decrease in testicular autophagy activity. The fertility of mutant mice was dramatically reduced with about 70% being infertile. Sperm counts and motility were also significantly reduced compared to controls. Histological examination of the mutant testes revealed numerous, large residual bodies in the lumen of stages after their normal resorption within the seminiferous epithelium. The cauda epididymal lumen was filled with sloughed germ cells, large cytoplasmic bodies, and spermatozoa with disorganized heads and tails. Examination of cauda epididymal sperm by electron microscopy revealed misshapen sperm heads, a discontinuous accessory structure in the mid-piece and abnormal acrosome formation and loss of sperm individualization. Immunofluorescence staining of epididymal sperm showed abnormal mitochondria and acrosome distribution in the mutant mice. ATG5 was shown to induce autophagy by mediating multiple signals to maintain normal developmental processes. Our study demonstrated ATG5 is essential for male fertility and is involved in various aspects of spermiogenesis. AKAP4: a-kinase anchoring protein 4; ATG5: autophagy-related 5; ATG7: autophagy-related 7; ATG10: autophagy-related 10; ATG12: autophagy-related 12; cKO: conditional knockout; DDX4: DEAD-box helicase 4; MAP1LC3/LC3/tg8: microtubule-associated protein 1 light chain 3; PBS: phosphate-buffered saline; PIWIL2/MILI: piwi like RNA-mediated gene silencing 2; RT-PCR: reverse transcription-polymerase chain reaction; SQSTM1/p62: sequestosome 1; TBC: tubulobulbar complexes; WT: wild type.
DOI: 10.6084/m9.figshare.12851405.v3
title: Autophagy core protein ATG5 is required for elongating spermatid development, sperm individualization and normal fertility in male mice

description: Spermiogenesis is the longest phase of spermatogenesis, with dramatic morphological changes and a final step of spermiation, which involves protein degradation and the removal of excess cytoplasm; therefore, we hypothesized that macroautophagy/autophagy might be involved in the process. To test this hypothesis, we examined the function of ATG5, a core autophagy protein in male germ cell development. Floxed <i>Atg5</i> and <i>Stra8− iCre</i> mice were crossed to conditionally inactivate <i>Atg5</i> in male germ cells. In <i>Atg5<sup>flox/flox</sup>; Stra8− iCre</i> mutant mice, testicular expression of the autophagosome marker LC3A/B-II was significantly reduced, and expression of autophagy receptor SQSTM1/p62 was significantly increased, indicating a decrease in testicular autophagy activity. The fertility of mutant mice was dramatically reduced with about 70% being infertile. Sperm counts and motility were also significantly reduced compared to controls. Histological examination of the mutant testes revealed numerous, large residual bodies in the lumen of stages after their normal resorption within the seminiferous epithelium. The cauda epididymal lumen was filled with sloughed germ cells, large cytoplasmic bodies, and spermatozoa with disorganized heads and tails. Examination of cauda epididymal sperm by electron microscopy revealed misshapen sperm heads, a discontinuous accessory structure in the mid-piece and abnormal acrosome formation and loss of sperm individualization. Immunofluorescence staining of epididymal sperm showed abnormal mitochondria and acrosome distribution in the mutant mice. ATG5 was shown to induce autophagy by mediating multiple signals to maintain normal developmental processes. Our study demonstrated ATG5 is essential for male fertility and is involved in various aspects of spermiogenesis. <b>Abbreviations</b>: AKAP4: a-kinase anchoring protein 4; ATG5: autophagy-related 5; ATG7: autophagy-related 7; ATG10: autophagy-related 10; ATG12: autophagy-related 12; cKO: conditional knockout; DDX4: DEAD-box helicase 4; MAP1LC3/LC3/tg8: microtubule-associated protein 1 light chain 3; PBS: phosphate-buffered saline; PIWIL2/MILI: piwi like RNA-mediated gene silencing 2; RT-PCR: reverse transcription-polymerase chain reaction; SQSTM1/p62: sequestosome 1; TBC: tubulobulbar complexes; WT: wild type.
DOI: 10.6084/m9.figshare.12851405.v2
title: Autophagy core protein ATG5 is required for elongating spermatid development, sperm individualization and normal fertility in male mice

description: Spermiogenesis is the longest phase of spermatogenesis, with dramatic morphological changes and a final step of spermiation, which involves protein degradation and the removal of excess cytoplasm; therefore, we hypothesized that macroautophagy/autophagy might be involved in the process. To test this hypothesis, we examined the function of ATG5, a core autophagy protein in male germ cell development. Floxed <i>Atg5</i> and <i>Stra8− iCre</i> mice were crossed to conditionally inactivate <i>Atg5</i> in male germ cells. In <i>Atg5<sup>flox/flox</sup>; Stra8− iCre</i> mutant mice, testicular expression of the autophagosome marker LC3A/B-II was significantly reduced, and expression of autophagy receptor SQSTM1/p62 was significantly increased, indicating a decrease in testicular autophagy activity. The fertility of mutant mice was dramatically reduced with about 70% being infertile. Sperm counts and motility were also significantly reduced compared to controls. Histological examination of the mutant testes revealed numerous, large residual bodies in the lumen of stages after their normal resorption within the seminiferous epithelium. The cauda epididymal lumen was filled with sloughed germ cells, large cytoplasmic bodies, and spermatozoa with disorganized heads and tails. Examination of cauda epididymal sperm by electron microscopy revealed misshapen sperm heads, a discontinuous accessory structure in the mid-piece and abnormal acrosome formation and loss of sperm individualization. Immunofluorescence staining of epididymal sperm showed abnormal mitochondria and acrosome distribution in the mutant mice. ATG5 was shown to induce autophagy by mediating multiple signals to maintain normal developmental processes. Our study demonstrated ATG5 is essential for male fertility and is involved in various aspects of spermiogenesis. <b>Abbreviations</b>: AKAP4: a-kinase anchoring protein 4; ATG5: autophagy-related 5; ATG7: autophagy-related 7; ATG10: autophagy-related 10; ATG12: autophagy-related 12; cKO: conditional knockout; DDX4: DEAD-box helicase 4; MAP1LC3/LC3/tg8: microtubule-associated protein 1 light chain 3; PBS: phosphate-buffered saline; PIWIL2/MILI: piwi like RNA-mediated gene silencing 2; RT-PCR: reverse transcription-polymerase chain reaction; SQSTM1/p62: sequestosome 1; TBC: tubulobulbar complexes; WT: wild type.
DOI: 10.6084/m9.figshare.12851411
title: PtdIns4P restriction by hydrolase SAC1 decides specific fusion of autophagosomes with lysosomes

description: Biogenesis of autophagosomes is the early step of macroautophagy/autophagy and requires membrane acquisition mainly from ER-Golgi-sourced precursor vesicles. Matured autophagosomes fuse with lysosomes for final degradation. However, how this selective fusion is determined remains elusive. Here, we identified Sac1 by a high throughput screen in <i>Saccharomyces cerevisiae</i> to show it was critical for autophagosome-lysosome fusion through its PtdIns4P phosphatase activity. Sac1 deficiency caused a dramatic increase of PtdIns4P at early Golgi apparatus and abnormal incorporation of PtdIns4P into Atg9 vesicles and autophagosomes, which caused failure to recruit SNARE proteins for autophagosome fusion with vacuoles. Sac1 function in autophagy was highly conserved from yeast to mammalian cells. Our work thus suggested that correct upstream lipid incorporation was important for downstream fusion step of autophagy and that Sac1 played a critical and ancient role in this surveillance of lipid integration. <b>Abbreviations:</b> Ape1: aminopeptidase Ι; ATG: autophagy related; EBSS: Earle’s balanced salt solution; ER: endoplasmic reticulum; ERGIC: Golgi apparatus and ER-Golgi intermediate compartment; HOPS: homotypic fusion and protein sorting complex; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; PtdIns3P: phosphatidylinositol-3-phosphate; PtdIns4K: phosphoinositide-4-kinase; PtdIns4P: phosphatidylinositol-4-phosphate; SD-N: nitrogen starvation medium; SNARE: soluble N-ethylamide-sensitive factor attachment protein receptor
DOI: 10.6084/m9.figshare.12851411.v1
title: PtdIns4P restriction by hydrolase SAC1 decides specific fusion of autophagosomes with lysosomes

description: Biogenesis of autophagosomes is the early step of macroautophagy/autophagy and requires membrane acquisition mainly from ER-Golgi-sourced precursor vesicles. Matured autophagosomes fuse with lysosomes for final degradation. However, how this selective fusion is determined remains elusive. Here, we identified Sac1 by a high throughput screen in <i>Saccharomyces cerevisiae</i> to show it was critical for autophagosome-lysosome fusion through its PtdIns4P phosphatase activity. Sac1 deficiency caused a dramatic increase of PtdIns4P at early Golgi apparatus and abnormal incorporation of PtdIns4P into Atg9 vesicles and autophagosomes, which caused failure to recruit SNARE proteins for autophagosome fusion with vacuoles. Sac1 function in autophagy was highly conserved from yeast to mammalian cells. Our work thus suggested that correct upstream lipid incorporation was important for downstream fusion step of autophagy and that Sac1 played a critical and ancient role in this surveillance of lipid integration. <b>Abbreviations:</b> Ape1: aminopeptidase Ι; ATG: autophagy related; EBSS: Earle’s balanced salt solution; ER: endoplasmic reticulum; ERGIC: Golgi apparatus and ER-Golgi intermediate compartment; HOPS: homotypic fusion and protein sorting complex; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; PtdIns3P: phosphatidylinositol-3-phosphate; PtdIns4K: phosphoinositide-4-kinase; PtdIns4P: phosphatidylinositol-4-phosphate; SD-N: nitrogen starvation medium; SNARE: soluble N-ethylamide-sensitive factor attachment protein receptor
DOI: 10.6084/m9.figshare.7608533
title: Additional file 1: of Proteomic analysis of the rice (Oryza officinalis) provides clues on molecular tagging of proteins for brown planthopper resistance

description: Table S1. List of 4907 identified proteins in BPH infested rice . (XLSX 610 kb)
DOI: 10.6084/m9.figshare.7608533.v1
title: Additional file 1: of Proteomic analysis of the rice (Oryza officinalis) provides clues on molecular tagging of proteins for brown planthopper resistance

description: Table S1. List of 4907 identified proteins in BPH infested rice . (XLSX 610 kb)
DOI: 10.6084/m9.figshare.12851417
title: Mice deficient in UXT exhibit retinitis pigmentosa-like features via aberrant autophagy activation

description: UXT (ubiquitously expressed prefoldin like chaperone), a small chaperone-like protein, is widely expressed in diverse human and mouse tissues and is more abundant in retina and kidney. However, the functional characterization of UXT at tissue level was largely unknown. Here, we reported that mice deficient in UXT exhibited salient features of retinal degenerative disease, similar to retinitis pigmentosa. Conditional knockout (CKO) of <i>Uxt</i> led to retinal degeneration and pigmentation in mice retina along with significant alterations of retinitis pigmentosa-related genes, which indicated UXT might be associated with retinal degenerative disease sharing key features to retinitis pigmentosa. Consistently, the electroretinogram (ERG) responses were dramatically impaired in <i>uxt</i> CKO retinas. Strong degenerative features were observed in <i>uxt</i> CKO retinas, including specific and progressive reduction of photoreceptor cells and increased numbers of apoptotic cells. Intriguingly, macroautophagic/autophagic ﬂux was enhanced in <i>uxt</i> CKO retina. Mechanistically, we found UXT was indispensable to suppress photoreceptor apoptotic cell death by inhibiting autophagy through regulating the activity of MTOR (mechanistic target of rapamycin kinase), a key negative regulator of autophagy. Conversely, knockdown of UXT induced the robust expression of the canonical autophagy-related genes and boosted autophagic ﬂux and apoptosis, finally resulting in severe retina degeneration in <i>uxt</i> CKO mice. Taken together, our study reveals a vital role of UXT in preventing retina from degeneration. The loss of UXT results in a hyper-autophagic state leading to massive retinal degeneration. Therefore, UXT may be a crucial target for retinal degenerative disease. <b>Abbreviations</b>: 3-ma: 3-methyladenine; casp3: caspase 3; cko: conditional knockout; erg: electroretinogram; gapdh: glyceraldehyde-3-phosphate dehydrogenase; map1lc3b/lc3b: microtubule-associated protein 1 light chain 3; mtor: mechanistic target of rapamycin kinase; parp: poly (adp-ribose) polymerase family; rna-seq: rna sequencing; rp: retinitis pigmentosa; rps6kb1/s6k: ribosomal protein s6 kinase b1; sqstm1: sequestosome 1; tunel: terminal deoxynucleotidyl transferase mediated dutp nick-end labeling; uxt: ubiquitously expressed prefoldin like chaperone.
DOI: 10.6084/m9.figshare.12851417.v1
title: Mice deficient in UXT exhibit retinitis pigmentosa-like features via aberrant autophagy activation

description: UXT (ubiquitously expressed prefoldin like chaperone), a small chaperone-like protein, is widely expressed in diverse human and mouse tissues and is more abundant in retina and kidney. However, the functional characterization of UXT at tissue level was largely unknown. Here, we reported that mice deficient in UXT exhibited salient features of retinal degenerative disease, similar to retinitis pigmentosa. Conditional knockout (CKO) of <i>Uxt</i> led to retinal degeneration and pigmentation in mice retina along with significant alterations of retinitis pigmentosa-related genes, which indicated UXT might be associated with retinal degenerative disease sharing key features to retinitis pigmentosa. Consistently, the electroretinogram (ERG) responses were dramatically impaired in <i>uxt</i> CKO retinas. Strong degenerative features were observed in <i>uxt</i> CKO retinas, including specific and progressive reduction of photoreceptor cells and increased numbers of apoptotic cells. Intriguingly, macroautophagic/autophagic ﬂux was enhanced in <i>uxt</i> CKO retina. Mechanistically, we found UXT was indispensable to suppress photoreceptor apoptotic cell death by inhibiting autophagy through regulating the activity of MTOR (mechanistic target of rapamycin kinase), a key negative regulator of autophagy. Conversely, knockdown of UXT induced the robust expression of the canonical autophagy-related genes and boosted autophagic ﬂux and apoptosis, finally resulting in severe retina degeneration in <i>uxt</i> CKO mice. Taken together, our study reveals a vital role of UXT in preventing retina from degeneration. The loss of UXT results in a hyper-autophagic state leading to massive retinal degeneration. Therefore, UXT may be a crucial target for retinal degenerative disease. <b>Abbreviations</b>: 3-ma: 3-methyladenine; casp3: caspase 3; cko: conditional knockout; erg: electroretinogram; gapdh: glyceraldehyde-3-phosphate dehydrogenase; map1lc3b/lc3b: microtubule-associated protein 1 light chain 3; mtor: mechanistic target of rapamycin kinase; parp: poly (adp-ribose) polymerase family; rna-seq: rna sequencing; rp: retinitis pigmentosa; rps6kb1/s6k: ribosomal protein s6 kinase b1; sqstm1: sequestosome 1; tunel: terminal deoxynucleotidyl transferase mediated dutp nick-end labeling; uxt: ubiquitously expressed prefoldin like chaperone.
DOI: 10.6084/m9.figshare.7608536
title: Additional file 4: of Integrated physiological and proteomic analysis of embryo and endosperm reveals central salt stress response proteins during seed germination of winter wheat cultivar Zhengmai 366

description: Table S4. Gene-specific primers used for RT-qPCR analysis. (XLSX 9 kb)
DOI: 10.6084/m9.figshare.7608536.v1
title: Additional file 4: of Integrated physiological and proteomic analysis of embryo and endosperm reveals central salt stress response proteins during seed germination of winter wheat cultivar Zhengmai 366

description: Table S4. Gene-specific primers used for RT-qPCR analysis. (XLSX 9 kb)
DOI: 10.6084/m9.figshare.7608539
title: Additional file 2: of Proteomic analysis of the rice (Oryza officinalis) provides clues on molecular tagging of proteins for brown planthopper resistance

description: Table S2. List of 414 differentially expressed proteins in BPH infested O. officinalis. (XLSX 35 kb)
DOI: 10.6084/m9.figshare.7608539.v1
title: Additional file 2: of Proteomic analysis of the rice (Oryza officinalis) provides clues on molecular tagging of proteins for brown planthopper resistance

description: Table S2. List of 414 differentially expressed proteins in BPH infested O. officinalis. (XLSX 35 kb)