<HashMap><database>biostudies-literature</database><scores><citationCount>0</citationCount><reanalysisCount>0</reanalysisCount><viewCount>38</viewCount><searchCount>0</searchCount></scores><additional><omics_type>Unknown</omics_type><volume>18(2)</volume><submitter>Yu D</submitter><pubmed_abstract>&lt;i>Fusarium graminearum&lt;/i> is the main causal agent of &lt;i>Fusarium&lt;/i> head blight (FHB) on wheat and barley. In a previous study, a GIN4-like protein kinase gene, &lt;i>GIL1&lt;/i>, was found to be important for plant infection and sexual reproduction. In this study we further characterized the functions of &lt;i>GIL1&lt;/i> kinase in different developmental processes. The Δ&lt;i>gil1&lt;/i> mutants were reduced in growth, conidiation, and virulence, and formed whitish and compact colonies. Although phialide formation was rarely observed in the mutants, deletion of &lt;i>GIL1&lt;/i> resulted in increased hyphal branching and increased tolerance to cell wall and cell membrane stresses. The Δ&lt;i>gil1&lt;/i> mutants produced straight, elongated conidia lacking of distinct foot cells and being delayed in germination. Compared with the wild type, some compartments in the vegetative hyphae of Δ&lt;i>gil1&lt;/i> mutants had longer septal distances and increased number of nuclei, suggesting &lt;i>GIL1&lt;/i> is related to cytokinesis and septation. Localization of the GIL1-GFP fusion proteins to the septum and hyphal branching and fusion sites further supported its roles in septation and branching. Overall, our results indicate that &lt;i>GIL1&lt;/i> plays a role in vegetative growth and plant infection in &lt;i>F. graminearum&lt;/i>, and is involved in septation and hyphal branching.</pubmed_abstract><journal>International journal of molecular sciences</journal><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5343958</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>A Gin4-Like Protein Kinase GIL1 Involvement in Hyphal Growth, Asexual Development, and Pathogenesis in Fusarium graminearum.</pubmed_title><pmcid>PMC5343958</pmcid><pubmed_authors>Li X</pubmed_authors><pubmed_authors>Jin Q</pubmed_authors><pubmed_authors>Xu JR</pubmed_authors><pubmed_authors>Yu D</pubmed_authors><pubmed_authors>Schultzhaus Z</pubmed_authors><pubmed_authors>Zhang S</pubmed_authors><view_count>38</view_count></additional><is_claimable>false</is_claimable><name>A Gin4-Like Protein Kinase GIL1 Involvement in Hyphal Growth, Asexual Development, and Pathogenesis in Fusarium graminearum.</name><description>&lt;i>Fusarium graminearum&lt;/i> is the main causal agent of &lt;i>Fusarium&lt;/i> head blight (FHB) on wheat and barley. In a previous study, a GIN4-like protein kinase gene, &lt;i>GIL1&lt;/i>, was found to be important for plant infection and sexual reproduction. In this study we further characterized the functions of &lt;i>GIL1&lt;/i> kinase in different developmental processes. The Δ&lt;i>gil1&lt;/i> mutants were reduced in growth, conidiation, and virulence, and formed whitish and compact colonies. Although phialide formation was rarely observed in the mutants, deletion of &lt;i>GIL1&lt;/i> resulted in increased hyphal branching and increased tolerance to cell wall and cell membrane stresses. The Δ&lt;i>gil1&lt;/i> mutants produced straight, elongated conidia lacking of distinct foot cells and being delayed in germination. Compared with the wild type, some compartments in the vegetative hyphae of Δ&lt;i>gil1&lt;/i> mutants had longer septal distances and increased number of nuclei, suggesting &lt;i>GIL1&lt;/i> is related to cytokinesis and septation. Localization of the GIL1-GFP fusion proteins to the septum and hyphal branching and fusion sites further supported its roles in septation and branching. Overall, our results indicate that &lt;i>GIL1&lt;/i> plays a role in vegetative growth and plant infection in &lt;i>F. graminearum&lt;/i>, and is involved in septation and hyphal branching.</description><dates><release>2017-01-01T00:00:00Z</release><publication>2017 Feb</publication><modification>2022-02-09T10:06:13.602Z</modification><creation>2019-03-27T02:38:17Z</creation></dates><accession>S-EPMC5343958</accession><cross_references><pubmed>28212314</pubmed><doi>10.3390/ijms18020424</doi></cross_references></HashMap>