The Caenorhabditis elegans gene ham-1 regulates daughter cell size asymmetry primarily in divisions that produce a small anterior daughter cell

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Abstract

C. elegans cell divisions that produce an apoptotic daughter cell exhibit Daughter Cell Size Asymmetry (DCSA), producing a larger surviving daughter cell and a smaller daughter cell fated to die. Genetic screens for mutants with defects in apoptosis identified several genes that are also required for the ability of these divisions to produce daughter cells that differ in size. One of these genes, ham-1, encodes a putative transcription factor that regulates a subset of the asymmetric cell divisions that produce an apoptotic daughter cell. In a survey of C. elegans divisions, we found that ham-1 mutations affect primarily anterior/posterior divisions that produce a small anterior daughter cell. The affected divisions include those that generate an apoptotic cell as well as those that generate two surviving cells. Our findings suggest that HAM-1 primarily promotes DCSA in a certain class of asymmetric divisions.

Figures

  • Table 1. ham-1 mutant extra cell phenotypes.
  • Fig 1. Automated lineaging of 13 neuroblast divisions that produce an apoptotic daughter cell. (A) Schematic representation of an embryo at 265 mins of development showing the positions of the 13 cells (or their daughters) whose divisions were analyzed. Cells are color-coded to describe which ones divide to produce an anterior daughter (blue) or posterior daughter (red) that dies. ABaraaaap (#7), which produces a posterior daughter that dies and whose division asymmetry is affected by ham-1 loss, is labelled in yellow. (B) Asymmetry ratios of all analyzed daughter cells in wild-type (green circles) and ham-1(gm279) (red circles) embryos. The name of the apoptotic cell (e.g., ABalaappaa) is represented along the X-axis with the corresponding number of daughter cells doublet used in (A). (C) A representative division of the ABalapapa cell (#3) yielding an anterior apoptotic daughter in wild-type (upper panel) and ham-1(gm279) (lower panel) embryos. Arrows indicate the two daughters, with anterior to the left. In the ham-1(gm279) mutant embryos, the asymmetry is reversed and reduced. The plasma membrane is labeled with pie-1::PH:: mCherry and the nucleus is visualized with his-72::HIS-72::GFP (REFs). Scale bars: 10 μm. (D, E) Comparison of asymmetry ratios for wild-type and ham-1(gm279) embryo to the time of chromatin compaction, a marker for apoptosis.
  • Fig 2. Abnormal numbers of neurons in nine neuroblast lineages that produce an anterior apoptotic daughter cell. (A) OLQDL, (B) ASKL/R, (C) URXL/R, (D) SMBVL/DL/DR, (E) MCL and (F) RICL/R lineage diagrams (upper panels) and the frequency of at least one extra neurons produced in wild-type (WT) and ham-1 mutant animals (lower panels). For each lineage, the neurons labelled are underlined on the diagram. Cells fated to die are indicated by an x, the anterior dying cell in each lineage is indicated by an x in a red square. The number of animals scored is indicated in parenthesis below each genotype.
  • Fig 3. Daughter cells size asymmetry (DCSA) defects in the ham-1 mutant T.pp and V5.paa divisions. (A) Schematic representation of the divisions in the T.p lineage. The T.pp division produces daughter cells of different fates and sizes, whereas the T.pa division produces daughter

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Teuliere, J., Kovacevic, I., Bao, Z., & Garriga, G. (2018). The Caenorhabditis elegans gene ham-1 regulates daughter cell size asymmetry primarily in divisions that produce a small anterior daughter cell. PLoS ONE, 13(4). https://doi.org/10.1371/journal.pone.0195855

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