A simple molecular mechanism explains multiple patterns of cell-size regulation

نویسندگان

  • Morgan Delarue
  • Daniel Weissman
  • Oskar Hallatschek
چکیده

Increasingly accurate and massive data have recently shed light on the fundamental question of how cells maintain a stable size trajectory as they progress through the cell cycle. Microbes seem to use strategies ranging from a pure sizer, where the end of a given phase is triggered when the cell reaches a critical size, to pure adder, where the cell adds a constant size during a phase. Yet the biological origins of the observed spectrum of behavior remain elusive. We analyze a molecular size-control mechanism, based on experimental data from the yeast S. cerevisiae, that gives rise to behaviors smoothly interpolating between adder and sizer. The size-control is obtained from the accumulation of an activator protein that titrates an inhibitor protein. Strikingly, the size-control is composed of two different regimes: for small initial cell size, the size-control is a sizer, whereas for larger initial cell size, it is an imperfect adder, in agreement with recent experiments. Our model thus indicates that the adder and critical size behaviors may just be different dynamical regimes of a single simple biophysical mechanism.

برای دانلود رایگان متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

MiR-9-5p and miR-106a-5p dysregulated in CD4+ T-cells of multiple sclerosis patients and targeted essential factors of T helper17/regulatory T-cells differentiation

Objective(s): Multiple sclerosis (MS) is considered as a chronic type of an inflammatory disease characterized by loss of myelin of CNS.Recent evidence indicates that Interleukin 17 (IL-17)-producing T helper cells (Th17 cells) population are increased and regulatory T cells (Treg cells) are decreased in MS. Despite extensive research in understanding the mechanism of Th17 and Treg differentiat...

متن کامل

Cabazitaxel antiproliferative mechanism of action in U87MG human glioblastoma cells: a promising cell-cycle phase-specific radiosensitizer

Introduction: One mechanism of cell cycle manipulation and mitotic catastrophe is arrest at G2/M phase of cell cycle. Cabazitaxel, a mitotic inhibitor agent, is a second-generation semisynthetic taxane. An expected anti-neoplastic effect of Cabazitaxel is cell cycle perturbation and alteration of microtubule dynamics. In contrast to other taxane compounds, Cabazitaxel is a poo...

متن کامل

Effects of Major Epigenetic Factors on Systemic Lupus Erythematosus

The pathogenesis of systemic lupus erythematosus (SLE) is influenced by both genetic factors and epigenetic modifications; the latter is a result of exposure to various environmental factors. Epigenetic modifications affect gene expression and alter cellular functions without modifying the genomic sequences. CpG-DNA methylation, histone modifications, and miRNAs are the main epigenetic factors ...

متن کامل

Epigallocatechin-3-Gallate Induces Apoptosis through Up-regulation of Bax and Down-regulation of Bcl-2 in Prostate Cancer Cell Line

Background and Aims: Epigallocatechin-3-gallate (EGCG) is a polyphenolic compound from green tea, which its anticancer effects on many types of cancers have been confirmed, but the molecular mechanism by which EGCG induces apoptosis remains unknown. The aim of the present study was to investigate anti-proliferative properties and apoptotic signaling pathway of EGCG on PC3 human prostate cancer ...

متن کامل

Nanocurcumin-Mediated Down-Regulation of Telomerase Via Stimulating TGFβ1 Signaling Pathway in Hepatocellular Carcinoma Cells

Background: Curcumin, extracted from turmeric, represents enormous potential to serve as an anticancer agent. Telomerase is viewed as a prominent molecular target of curcumin, and transforming growth factor-β1 (TGFβ1) has proven to be a major inhibitory signaling pathway for telomerase activity. In the current study, we aimed to explore suppressive effects of nanocurcumin on telomeras...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

عنوان ژورنال:

دوره 12  شماره 

صفحات  -

تاریخ انتشار 2017