Cohesin is an evolutionarily conserved protein complex that plays a role in many biological processes: it ensures faithful chromosome segregation, regulates gene expression and preserves genome stability. In mammalian cells, the mitotic cohesin complex consists of two structural maintenance of chromosome proteins, SMC1A and SMC3, the kleisin protein RAD21 and a fourth subunit either STAG1 or STAG2. Meiotic paralogs in mammals were reported for SMC1A, RAD21 and STAG1/STAG2 and are called SMC1B, REC8 and STAG3 respectively. It is believed that SMC1B is only a meiotic-specific cohesin member, required for sister chromatid pairing and for preventing telomere shortening. Here we show that SMC1B is also expressed in somatic mammalian cells and is a member of a mitotic cohesin complex. In addition, SMC1B safeguards genome stability following irradiation whereas its ablation has no effect on chromosome segregation. Finally, unexpectedly SMC1B depletion impairs gene transcription, particularly at genes mapping to clusters such as HOX and PCDHB. Genome-wide analyses show that cluster genes changing in expression are enriched for cohesin-SMC1B binding.
A combination of three superheated drop detectors with different neutron energy responses was developed to evaluate dose-equivalent and energy distributions of photoneutrons in a phantom irradiated by radiotherapy high-energy x-ray beams. One of the three detectors measures the total neutron dose equivalent and the other two measure the contributions from fast neutrons above 1 and 5.5 MeV, respectively. In order to test the new method, the neutron field produced by the 10 cm X 10 cm x-ray beam of an 18 MV radiotherapy accelerator was studied. Measurements were performed inside a tissue-equivalent liquid phantom, at depths of 1, 5, 10 and 15 cm and at lateral distances of 0, 10, and 20 cm from the central axis. These data were used to calculate the average integral dose to the radiotherapy patient from direct neutrons as well as from neutrons transmitted through the accelerator head. The characteristics of the dosimeters were confirmed by results in excellent agreement with those of prior studies. Track etch detectors were also used and provided an independent verification of the validity of this new technique. Within the primary beam, we measured a neutron entrance dose equivalent of 4.5 mSv per Gy of photons. It was observed that fast neutrons above 1 MeV deliver most of the total neutron dose along the beam axis. Their relative contribution increases with depth, from about 60% at the entrance to over 90% at a depth of 10 cm. Thus, the average energy increases with depth in the phantom as neutron spectra harden.
Prohibitins are pleiotropic proteins, whose multiple roles are emerging as key elements in the regulation of cell survival and proliferation. Indeed, prohibitins interact with several intracellular proteins strategically involved in the regulation of cell cycle progression in response to extracellular growth signals. Prohibitins also have regulatory functions in mitochondrial fusion and cristae morphogenesis, phenomena related to the ability of self-renewing embryonic stem cells to undergo differentiation, during which mitochondria develop numerous cristae, increase in number, and generate an extensive reticular network. We recently identified a Prohibitin 2 homolog (DjPhb2) that is expressed in adult stem cells (neoblasts) of planarians, a well-known model system for in vivo studies on stem cells and tissue regeneration. Here, we show that in DjPhb2 silenced planarians, most proliferating cells disappear, with the exception of a subpopulation of neoblasts localized along the dorsal body midline. Neoblast depletion impairs regeneration and, finally, leads animals to death. Our in vivo findings demonstrate that prohibitin 2 plays an important role in regulating stem cell biology, being involved in both the control of cell cycle progression and mitochondrial cristae morphogenesis.
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