Observation of RIN reduction via spectral broadening in an NPR-based stretched pulse fiber laser.

We show that an optimum mode-locking state with low relative intensity noise (RIN) can be identified by continuous broadening of an optical spectrum in a stretched-pulse fiber laser based on nonlinear polarization rotation (NPR). Under the premise of keeping the overall spectral shape unchanged, either gradually increasing the pump power or unidirectionally adjusting the polarization controller (PC) can effectively reduce RIN as the optical spectral bandwidth broadens. The optimized intensity noise performance of the laser can be attributed to the increased pulse energy and reduced intra-cavity net dispersion. Moreover, the integrated RIN will further decrease as the maximum 3-dB bandwidth extends. In our experiment, the detected minimum integrated rms RIN is below 0.003% (from 100 Hz to 100 kHz). Our experimental results find that the absolute spectral width is not a necessary key condition for obtaining low RIN mode-locked laser, whereas it may help understand and design versatile low-noise ultrafast laser sources.

A novel recombination protein C12ORF40/REDIC1 is required for meiotic crossover formation.

During meiosis, at least one crossover must occur per homologous chromosome pair to ensure normal progression of meiotic division and accurate chromosome segregation. However, the mechanism of crossover formation is not fully understood. Here, we report a novel recombination protein, C12ORF40/REDIC1, essential for meiotic crossover formation in mammals. A homozygous frameshift mutation in C12orf40 (c.232_233insTT, p.Met78Ilefs*2) was identified in two infertile men with meiotic arrest. Spread mouse spermatocyte fluorescence immunostaining showed that REDIC1 forms discrete foci between the paired regions of homologous chromosomes depending on strand invasion and colocalizes with MSH4 and later with MLH1 at the crossover sites. Redic1 knock-in (KI) mice homozygous for mutation c.232_233insTT are infertile in both sexes due to insufficient crossovers and consequent meiotic arrest, which is also observed in our patients. The foci of MSH4 and TEX11, markers of recombination intermediates, are significantly reduced numerically in the spermatocytes of Redic1 KI mice. More importantly, our biochemical results show that the N-terminus of REDIC1 binds branched DNAs present in recombination intermediates, while the identified mutation impairs this interaction. Thus, our findings reveal a crucial role for C12ORF40/REDIC1 in meiotic crossover formation by stabilizing the recombination intermediates, providing prospective molecular targets for the clinical diagnosis and therapy of infertility.