Partition of protein (mass) to sister cell pairs at mitosis: a re-evaluation.

نویسنده

  • R Sennerstam
چکیده

Since the 1960s it has been thought that there is to some extent a difference in the partition of mass to daughter cells at mitosis. Recent studies using modern techniques give further support to such a phenomenon, which has become almost an axiom in cell biology. It has been suggested that such unequal distribution of metabolic constituents at mitosis contributes to the dispersion in cell generation times. In the present work, PCC3 embryonal carcinoma (EC) cells were studied as undifferentiated G1 sister pairs by microspectrophotometry (MSP) following Feulgen-Naphthol Yellow staining (FNYS), in order to evaluate their protein content. Despite the considerable intraclonal intermitotic time heterogeneity found in undifferentiated PCC3 EC cells, it was concluded thta the postmitotic difference in mass (protein) between sister cell pairs exerts a minimal influence upon the cell population mass variability, whereas it was deduced to have an influence upon variation in interphase time duration when comparing sister cell pairs. This offers a cell-physiological explanation to the randomly distributed difference repeatedly found between sister cell generation times. Furthermore, there was no correlation seen between the mass difference found between sister cell pairs postmitotically and the size of the mother cell.

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

Bub1 multitasking in mitosis.

Accurate partition of duplicated genetic material to the daughter cells during mitosis relies on the maintenance of the physical linkage (cohesion) between sister chromatids until their bipolar attachment to the mitotic spindle. In response to a single straying chromatid within a cell, a surveillance mechanism called the spindle checkpoint blocks the ubiquitin ligase activity of the anaphase-pr...

متن کامل

The mechanism of sister chromatid cohesion.

Each of our cells inherit their genetic information in the form of chromosomes from a mother cell. In order that we obtain the full genetic complement, cells need to ensure that replicated chromosomes are accurately split and distributed during cell division. Mistakes in this process lead to aneuploidies, cells with supernumerous or missing chromosomes. Most aneuploid human embryos are not viab...

متن کامل

Downregulation of Kinesin Spindle Protein Inhibits Proliferation, Induces Apoptosis and Increases Chemosensitivity in Hepatocellular Carcinoma Cells

Background: Kinesin spindle protein (KSP) plays a critical role in mitosis. Inhibition of KSP function leads to cell cycle arrest at mitosis and ultimately to cell death. The aim of this study was to suppress KSP expression by specific small-interfering RNA (siRNA) in Hep3B cells and evaluate its anti-tumor activity. Methods: Three siRNA targeting KSP (KSP-siRNA #1-3) and one mismatched-siRNA (...

متن کامل

The Monopolin Complex Crosslinks Kinetochore Components to Regulate Chromosome-Microtubule Attachments

The monopolin complex regulates different types of kinetochore-microtubule attachments in fungi, ensuring sister chromatid co-orientation in Saccharomyces cerevisiae meiosis I and inhibiting merotelic attachment in Schizosaccharomyces pombe mitosis. In addition, the monopolin complex maintains the integrity and silencing of ribosomal DNA (rDNA) repeats in the nucleolus. We show here that the S....

متن کامل

Sister chromatid cohesion and genome stability in vertebrate cells.

For successful eukaryotic mitosis, sister chromatid pairs remain linked after replication until their kinetochores have been attached to opposite spindle poles by microtubules. This linkage is broken at the metaphase-anaphase transition and the sisters separate. In budding yeast, this sister chromatid cohesion requires a multi-protein complex called cohesin. A key component of cohesin is Scc1/M...

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:
  • Journal of cell science

دوره 90 ( Pt 2)  شماره 

صفحات  -

تاریخ انتشار 1988