Robust estimation of bacterial cell count from optical density

Optical density (OD) is widely used to estimate the density of cells in liquid culture, but cannot be compared between instruments without a standardized calibration protocol and is challenging to relate to actual cell count. We address this with an interlaboratory study comparing three simple, low-cost, and highly accessible OD calibration protocols across 244 laboratories, applied to eight strains of constitutive GFP-expressing E. coli. Based on our results, we recommend calibrating OD to estimated cell count using serial dilution of silica microspheres, which produces highly precise calibration (95.5% of residuals <1.2-fold), is easily assessed for quality control, also assesses instrument effective linear range, and can be combined with fluorescence calibration to obtain units of Molecules of Equivalent Fluorescein (MEFL) per cell, allowing direct comparison and data fusion with flow cytometry measurements: in our study, fluorescence per cell measurements showed only a 1.07-fold mean difference between plate reader and flow cytometry data

The New Age of Hyperspectral Oceanography

A multispectral optical sensor collects data at select wavebands or channels. An example is the Sea-viewing Wide-Field-of-view Sensor (SeaWiFS) ocean color satellite, which measures eight wavebands between 402 and 885 nm (20-40 nm bandwidth with peaks centered around 412, 443, 490, 510, 555, 670, 765, and 865 nm). Optical oceanographers have been using multispectral sensors since the 1980s with great success

The New Age of Hyperspectral Oceanography

A multispectral optical sensor collects data at select wavebands or channels. An example is the Sea-viewing Wide-Field-of-view Sensor (SeaWiFS) ocean color satellite, which measures eight wavebands between 402 and 885 nm (20-40 nm bandwidth with peaks centered around 412, 443, 490, 510, 555, 670, 765, and 865 nm). Optical oceanographers have been using multispectral sensors since the 1980s with great success.Keywords: ocean optics\, oceanograph

CLN8 is an endoplasmic reticulum cargo receptor that regulates lysosome biogenesis

Organelle biogenesis requires proper transport of proteins from their site of synthesis to their target subcellular compartment1-3. Lysosomal enzymes are synthesized in the endoplasmic reticulum (ER) and traffic through the Golgi complex before being transferred to the endolysosomal system4-6, but how they are transferred from the ER to the Golgi is unknown. Here, we show that ER-to-Golgi transfer of lysosomal enzymes requires CLN8, an ER-associated membrane protein whose loss of function leads to the lysosomal storage disorder, neuronal ceroid lipofuscinosis 8 (a type of Batten disease)7. ER-to-Golgi trafficking of CLN8 requires interaction with the COPII and COPI machineries via specific export and retrieval signals localized in the cytosolic carboxy terminus of CLN8. CLN8 deficiency leads to depletion of soluble enzymes in the lysosome, thus impairing lysosome biogenesis. Binding to lysosomal enzymes requires the second luminal loop of CLN8 and is abolished by some disease-causing mutations within this region. Our data establish an unanticipated example of an ER receptor serving the biogenesis of an organelle and indicate that impaired transport of lysosomal enzymes underlies Batten disease caused by mutations in CLN8

CLN8 is an endoplasmic reticulum cargo receptor that regulates lysosome biogenesis

Organelle biogenesis requires proper transport of proteins from their site of synthesis to their target subcellular compartment1-3. Lysosomal enzymes are synthesized in the endoplasmic reticulum (ER) and traffic through the Golgi complex before being transferred to the endolysosomal system4-6, but how they are transferred from the ER to the Golgi is unknown. Here, we show that ER-to-Golgi transfer of lysosomal enzymes requires CLN8, an ER-associated membrane protein whose loss of function leads to the lysosomal storage disorder, neuronal ceroid lipofuscinosis 8 (a type of Batten disease)7. ER-to-Golgi trafficking of CLN8 requires interaction with the COPII and COPI machineries via specific export and retrieval signals localized in the cytosolic carboxy terminus of CLN8. CLN8 deficiency leads to depletion of soluble enzymes in the lysosome, thus impairing lysosome biogenesis. Binding to lysosomal enzymes requires the second luminal loop of CLN8 and is abolished by some disease-causing mutations within this region. Our data establish an unanticipated example of an ER receptor serving the biogenesis of an organelle and indicate that impaired transport of lysosomal enzymes underlies Batten disease caused by mutations in CLN8

Measurement of the branching fractions for Cabibbo-suppressed decays D+→K+K−π+π0D^{+}\to K^{+} K^{-}\pi^{+}\pi^{0} and D(s)+→K+π−π+π0D_{(s)}^{+}\to K^{+}\pi^{-}\pi^{+}\pi^{0} at Belle

International audienceWe present measurements of the branching fractions for the singly Cabibbo-suppressed decays $D^+\to K^{+}K^{-}\pi^{+}\pi^{0}$ and $D_s^{+}\to K^{+}\pi^{-}\pi^{+}\pi^{0}$, and the doubly Cabibbo-suppressed decay $D^{+}\to K^{+}\pi^{-}\pi^{+}\pi^{0}$, based on 980 ${\rm fb}^{-1}$ of data recorded by the Belle experiment at the KEKB $e^{+}e^{-}$ collider. We measure these modes relative to the Cabibbo-favored modes $D^{+}\to K^{-}\pi^{+}\pi^{+}\pi^{0}$ and $D_s^{+}\to K^{+}K^{-}\pi^{+}\pi^{0}$. Our results for the ratios of branching fractions are $B(D^{+}\to K^{+}K^{-}\pi^{+}\pi^{0})/B(D^{+}\to K^{-}\pi^{+}\pi^{+}\pi^{0}) = (11.32 \pm 0.13 \pm 0.26)\%$, $B(D^{+}\to K^{+}\pi^{-}\pi^{+}\pi^{0})/B(D^{+}\to K^{-}\pi^{+}\pi^{+}\pi^{0}) = (1.68 \pm 0.11\pm 0.03)\%$, and $B(D_s^{+}\to K^{+}\pi^{-}\pi^{+}\pi^{0})/B(D_s^{+}\to K^{+}K^{-}\pi^{+}\pi^{0}) = (17.13 \pm 0.62 \pm 0.51)\%$, where the uncertainties are statistical and systematic, respectively. The second value corresponds to $(5.83\pm 0.42)\times\tan^4\theta_C$, where $\theta_C$ is the Cabibbo angle; this value is larger than other measured ratios of branching fractions for a doubly Cabibbo-suppressed charm decay to a Cabibbo-favored decay. Multiplying these results by world average values for $B(D^{+}\to K^{-}\pi^{+}\pi^{+}\pi^{0})$ and $B(D_s^{+}\to K^{+}K^{-}\pi^{+}\pi^{0})$ yields $B(D^{+}\to K^{+}K^{-}\pi^{+}\pi^{0})= (7.08\pm 0.08\pm 0.16\pm 0.20)\times10^{-3}$, $B(D^{+}\to K^{+}\pi^{-}\pi^{+}\pi^{0})= (1.05\pm 0.07\pm 0.02\pm 0.03)\times10^{-3}$, and $B(D_s^{+}\to K^{+}\pi^{-}\pi^{+}\pi^{0}) = (9.44\pm 0.34\pm 0.28\pm 0.32)\times10^{-3}$, where the third uncertainty is due to the branching fraction of the normalization mode. The first two results are consistent with, but more precise than, the current world averages. The last result is the first measurement of this branching fraction

Measurement of the B+/B0B^+/B^0 production ratio in e+e−e^+e^- collisions at the Υ(4S)\Upsilon(4S) resonance using B→J/ψ(ℓℓ)KB \rightarrow J/\psi(\ell\ell) K decays at Belle

We measure the ratio of branching fractions for the $\Upsilon (4S)$ decays to $B^+B^-$ and $B^0\bar{B}{}^0$ using $B^+ \rightarrow J/\psi(\ell\ell) K^+$ and $B^0 \rightarrow J/\psi(\ell\ell) K^0$ samples, where $J/\psi(\ell\ell)$ stands for $J/\psi \to \ell^+\ell^-$ ($\ell = e$ or $\mu$), with $711$ fb$^{-1}$ of data collected at the $\Upsilon(4S)$ resonance with the Belle detector. We find the decay rate ratio of $\Upsilon(4S) \rightarrow B^+B^-$ over $\Upsilon(4S) \rightarrow B^0\bar{B}{}^0$ to be $1.065\pm0.012\pm 0.019 \pm 0.047$, which is the most precise measurement to date. The first and second uncertainties are statistical and systematic, respectively, and the third uncertainty is systematic due to the assumption of isospin symmetry in $B \to J/\psi(\ell\ell) K$

Measurement of branching fractions of Λc+→pKS0KS0\Lambda_c^+\to{}pK_S^0K_S^0 and Λc+→pKS0η\Lambda_c^+\to{}pK_S^0\eta at Belle

We present a study of a singly Cabibbo-suppressed decay $\Lambda_c^+\to{}pK_S^0K_S^0$ and a Cabibbo-favored decay $\Lambda_c^+\to{}pK_S^0\eta$ based on 980 $\rm fb^{-1}$ of data collected by the Belle detector, operating at the KEKB energy-asymmetric $e^+e^-$ collider. We measure their branching fractions relative to $\Lambda_c^+\to{}pK_S^0$: $\mathcal{B}(\Lambda_c^+\to{}pK_S^0K_S^0)/\mathcal{B}(\Lambda_c^+\to{}pK_S^0)={(1.48 \pm 0.08 \pm 0.04)\times 10^{-2}}$ and $\mathcal{B}(\Lambda_c^+\to{}pK_S^0\eta)/\mathcal{B}(\Lambda_c^+\to{}pK_S^0)={(2.73\pm 0.06\pm 0.13)\times 10^{-1}}$. Combining with the world average $\mathcal{B}(\Lambda_c^+\to{}pK_S^0)$, we have the absolute branching fractions: $\mathcal{B}(\Lambda_c^+\to{}pK_S^0K_S^0) = {(2.35\pm 0.12\pm 0.07 \pm 0.12 )\times 10^{-4}}$ and $\mathcal{B}(\Lambda_c^+\to{}pK_S^0\eta) = {(4.35\pm 0.10\pm 0.20 \pm 0.22 )\times 10^{-3}}$. The first and second uncertainties are statistical and systematic, respectively, while the third ones arise from the uncertainty on $\mathcal{B}(\Lambda_c^+\to{}pK_S^0)$. The mode $\Lambda_c^+\to{}pK_S^0K_S^0$ is observed for the first time and has a statistical significance of $>\!10\sigma$. The branching fraction of $\Lambda_c^+\to{}pK_S^0\eta$ has been measured with a threefold improvement in precision over previous results and is found to be consistent with the world average