<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Liaqat A</submitter><funding>Chinese Government Scholarship</funding><funding>China Postdoctoral Science Foundation</funding><funding>National Natural Science Foundation of China</funding><funding>CAS-TWAS President’s Fellowship</funding><pagination>49</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9869573</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>23(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Salt stress significantly influences plant growth and reduces crop yield. It is highly anticipated to develop salt-tolerant crops with salt tolerance genes and transgenic technology. Hence, it is critical to identify salt tolerance genes that can be used to improve crop salt tolerance.&lt;h4>Results&lt;/h4>We report that the transcription elongation factor suppressor of Ty 4-2 (SPT4-2) is a positive modulator of salt tolerance in Arabidopsis thaliana. AtSPT4-2 expression is induced by salt stress. Knockout mutants of AtSPT4-2 display a salt-sensitive phenotype, whereas AtSPT4-2 overexpression lines exhibit enhanced salt tolerance. Comparative transcriptomic analyses revealed that AtSPT4-2 may orchestrate the expression of genes associated with salt tolerance, including stress-responsive markers, protein kinases and phosphatases, salt-responsive transcription factors and those maintaining ion homeostasis, suggesting that AtSPT4-2 improves salt tolerance mainly by maintaining ion homeostasis and enhancing stress tolerance.&lt;h4>Conclusions&lt;/h4>AtSPT4-2 positively modulates salt tolerance by maintaining ion homeostasis and regulating stress-responsive genes and serves as a candidate for the improvement of crop salt tolerance.</pubmed_abstract><journal>BMC plant biology</journal><pubmed_title>Transcription elongation factor AtSPT4-2 positively modulates salt tolerance in Arabidopsis thaliana.</pubmed_title><pmcid>PMC9869573</pmcid><funding_grant_id>2020T130634</funding_grant_id><funding_grant_id>31900230</funding_grant_id><pubmed_authors>Sun L</pubmed_authors><pubmed_authors>Liaqat A</pubmed_authors><pubmed_authors>Zhao P</pubmed_authors><pubmed_authors>Xiang C</pubmed_authors><pubmed_authors>Alfatih A</pubmed_authors><pubmed_authors>Jan SU</pubmed_authors></additional><is_claimable>false</is_claimable><name>Transcription elongation factor AtSPT4-2 positively modulates salt tolerance in Arabidopsis thaliana.</name><description>&lt;h4>Background&lt;/h4>Salt stress significantly influences plant growth and reduces crop yield. It is highly anticipated to develop salt-tolerant crops with salt tolerance genes and transgenic technology. Hence, it is critical to identify salt tolerance genes that can be used to improve crop salt tolerance.&lt;h4>Results&lt;/h4>We report that the transcription elongation factor suppressor of Ty 4-2 (SPT4-2) is a positive modulator of salt tolerance in Arabidopsis thaliana. AtSPT4-2 expression is induced by salt stress. Knockout mutants of AtSPT4-2 display a salt-sensitive phenotype, whereas AtSPT4-2 overexpression lines exhibit enhanced salt tolerance. Comparative transcriptomic analyses revealed that AtSPT4-2 may orchestrate the expression of genes associated with salt tolerance, including stress-responsive markers, protein kinases and phosphatases, salt-responsive transcription factors and those maintaining ion homeostasis, suggesting that AtSPT4-2 improves salt tolerance mainly by maintaining ion homeostasis and enhancing stress tolerance.&lt;h4>Conclusions&lt;/h4>AtSPT4-2 positively modulates salt tolerance by maintaining ion homeostasis and regulating stress-responsive genes and serves as a candidate for the improvement of crop salt tolerance.</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Jan</publication><modification>2025-04-26T17:23:21.825Z</modification><creation>2025-02-19T03:00:16.107Z</creation></dates><accession>S-EPMC9869573</accession><cross_references><pubmed>36683032</pubmed><doi>10.1186/s12870-023-04060-x</doi></cross_references></HashMap>