Fhod1, an actin-organizing formin family protein, is dispensable for cardiac development and function in mice

Fumiyuki Sanematsu, Ami Kanai, Tomoki Ushijima, Aki Shiraishi, Takaya Abe, Yohko Kage, Hideki Sumimoto, Ryu Takeya

研究成果: Contribution to journalArticle査読

4 被引用数 (Scopus)

抄録

The formin family proteins have the ability to regulate actin filament assembly, thereby functioning in diverse cytoskeletal processes. Fhod3, a cardiac member of the family, plays a crucial role in development and functional maintenance of the heart. Although Fhod1, a protein closely-related to Fhod3, has been reported to be expressed in cardiomyocytes, the role of Fhod1 in the heart has still remained elusive. To know the physiological role of Fhod1 in the heart, we disrupted the Fhod1 gene in mice by replacement of exon 1 with a lacZ reporter gene. Histological lacZ staining unexpectedly revealed no detectable expression of Fhod1 in the heart, in contrast to intensive staining in the lung, a Fhod1-containing organ. Consistent with this, expression level of the Fhod1 protein in the heart was below the lower limit of detection of the present immunoblot analysis with three independent anti-Fhod1 antibodies. Homozygous Fhod1-null mice did not show any defects in gross and histological appearance of the heart or upregulate fetal cardiac genes that are induced under stress conditions. Furthermore, Fhod1 ablation did not elicit compensatory increase in expression of other formins. Thus, Fhod1 appears to be dispensable for normal development and function of the mouse heart, even if a marginal amount of Fhod1 is expressed in the heart.

本文言語英語
ページ(範囲)219-229
ページ数11
ジャーナルCytoskeleton
76
2
DOI
出版ステータス出版済み - 2 1 2019
外部発表はい

All Science Journal Classification (ASJC) codes

  • Structural Biology
  • Cell Biology

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