Photography-based taxonomy is inadequate, unnecessary, and potentially harmful for biological sciences

The question whether taxonomic descriptions naming new animal species without type specimen(s) deposited in collections should be accepted for publication by scientific journals and allowed by the Code has already been discussed in Zootaxa (Dubois & Nemésio 2007; Donegan 2008, 2009; Nemésio 2009a–b; Dubois 2009; Gentile & Snell 2009; Minelli 2009; Cianferoni & Bartolozzi 2016; Amorim et al. 2016). This question was again raised in a letter supported by 35 signatories published in the journal Nature (Pape et al. 2016) on 15 September 2016. On 25 September 2016, the following rebuttal (strictly limited to 300 words as per the editorial rules of Nature) was submitted to Nature, which on 18 October 2016 refused to publish it. As we think this problem is a very important one for zoological taxonomy, this text is published here exactly as submitted to Nature, followed by the list of the 493 taxonomists and collection-based researchers who signed it in the short time span from 20 September to 6 October 2016

A Molecular Analysis of the Na +

The homologous genes encoding the electroneutral solute carrier family 12A (SLC12A) were identified more than 20 years ago, however, over the last few years, it has become clear that each of the genes within this family potentially encode for more than one cation-chloride cotransporter (CCC). Even more surprising, despite more than 30 years of functional studies and a wealth of knowledge on the activators, inhibitors, ion affinities, and kinetics of these cotransporters, we still cannot sufficiently explain why some cells express only one CCC isoform, while others express two, three, or more CCC isoforms. In 2009, Drs. Alvarez-Leefmans and Di Fulvio published an extensive in silico molecular analysis of the potential splice variants of the Na+-dependent cation-chloride cotransporters. In this review, we will look at the exceptionally large variety of potential splice variants within the Na+-independent cation-chloride cotransporter (SLC12A4-SLC12A7) genes, their initial tissue identification, and their physiological relevance

The feeding microstructure of male and female mice.

The feeding pattern and control of energy intake in mice housed in groups are poorly understood. Here, we determined and quantified the normal feeding microstructure of social male and female mice of the C57BL/6J genetic background fed a chow diet. Mice at 10w, 20w and 30w of age showed the expected increase in lean and fat mass, being the latter more pronounced and variable in males than in females. Under ad libitum conditions, 20w and 30w old females housed in groups showed significantly increased daily energy intake when adjusted to body weight relative to age-matched males. This was the combined result of small increases in energy intake during the nocturnal and diurnal photoperiods of the day without major changes in the circadian pattern of energy intake or spontaneous ambulatory activity. The analysis of the feeding microstructure suggests sex- and age-related contributions of meal size, meal frequency and intermeal interval to the control of energy intake under stable energy balance, but not under negative energy balance imposed by prolonged fasting. During the night, 10-20w old females ate less frequently bigger meals and spent more time eating them resulting in reduced net energy intake relative to age-matched males. In addition, male and female mice at all ages tested significantly shortened the intermeal interval during the first hours of re-feeding in response to fasting without affecting meal size. Further, 20-30w old males lengthened their intermeal interval as re-feeding time increased to reach fed-levels faster than age-matched females. Collectively, our results suggest that the physiological mechanisms controlling meal size (satiation) and the non-eating time spent between meals (satiety) during stable or negative energy balance are regulated in a sex- and age-dependent manner in social mice

Expression of the \u3cem\u3eSlc12a1\u3c/em\u3e Gene in Pancreatic β-Cells: Molecular Characterization and \u3cem\u3ein silico\u3c/em\u3e Analysis

The solute carrier protein family 12 group A, member one (Slc12a1) and two (Slc12a2) encode several splice variants of the kidney-specific and the ubiquitous isoforms, respectively, of the bumetanide (BTD)-sensitive Na-dependent K2Cl co-transporter. The Slc12a2 co-transporter is involved in the maintenance of a high intracellular chloride concentration [Cl–]i in β-cells and its inhibition with BTD blocks glucose-induced insulin secretion. In β-cells, [Cl–]i plays an important role in glucose-induced depolarization and insulin secretion. Glucose promotes electrogenic efflux of Cl– contributing to β-cell\u27s electrical and secretory activity. To identify the expression pattern of Slc12a1 and Slc12a2 genes in β-cells we have used RT-PCR, Western blotting and immunolocalization studies in mouse pancreatic islets, β-cell lines and rat tissues. Our results demonstrate expression of specific splice variants of Slc12a1 and Slc12a2 transcripts in β-cells i.e., variants 1 of Slc12a1 (NKCC2A) and Slc12a2 (NKCC1a). Molecular cloning and characterization of Slc12a1 variant 1 transcripts from β-cells revealed an alternative splicing event involving the 5\u27-UTR region. NKCC2A expression at the protein level in islets and β-cells was confirmed by immunoblotting and immunolocalization. Further, NKCC2A, NKCC1a and pro-insulin co-localized in β-cells but not in the exocrine pancreas. Therefore, our results provide for the first time evidence of NKCC2A expression in pancreatic β-cells where it may play a role in insulin secretion

Expression of the NKCC2A Cotransporter in Mouse Central Nervous System

Na-K-2Cl cotransporter 2A (NKCC2A), also known as the bumetanide-sensitive cotransporter 1 (BSC1), transports Na+, K+ and Cl- with a stoichiometry of 1:1:2. NKCC2A is considered a kidney specific cotransporter. It is abundantly expressed in apical membrane of the tubular cells in the thick ascending limb of the loop of Henle (TALH) and in the macula densa. However, NKCC2 has also been found at low levels in different cells, including insulin-secreting ones. This secondary active transporter uses the energy stored in the electrochemical gradients of Na and K maintained by the Na/K-ATPase located on the basolateral membrane of the TALH. The gene encoding NKCC2 is Slc12a1, solute carrier family 12 member 1 located on chromosome 2. Mice lacking NKCC2A (NKCC2A-KO) exhibit mild kidney dysfunction. In this lab it was noted that NKCC2A-KO mice express atypical muscle movements, slight tremors and subtle muscle dyscontrol, endure exceptionally well in the forced swim test and had changes in neurotransmitter levels. These observations led to the hypothesis that NKCC2A may be also found in the central nervous system (CNS).https://corescholar.libraries.wright.edu/urop_celebration/1013/thumbnail.jp

Impact of Hybrid and Complex N-Glycans on Cell Surface Targeting of the Endogenous Chloride Cotransporter Slc12a2

The Na+K+2Cl− cotransporter-1 (Slc12a2, NKCC1) is widely distributed and involved in cell volume/ion regulation. Functional NKCC1 locates in the plasma membrane of all cells studied, particularly in the basolateral membrane of most polarized cells. Although the mechanisms involved in plasma membrane sorting of NKCC1 are poorly understood, it is assumed that N-glycosylation is necessary. Here, we characterize expression, N-glycosylation, and distribution of NKCC1 in COS7 cells. We show that ~25% of NKCC1 is complex N-glycosylated whereas the rest of it corresponds to core/high-mannose and hybrid-type N-glycosylated forms. Further, ~10% of NKCC1 reaches the plasma membrane, mostly as core/high-mannose type, whereas ~90% of NKCC1 is distributed in defined intracellular compartments. In addition, inhibition of the first step of N-glycan biosynthesis with tunicamycin decreases total and plasma membrane located NKCC1 resulting in almost undetectable cotransport function. Moreover, inhibition of N-glycan maturation with swainsonine or kifunensine increased core/hybrid-type NKCC1 expression but eliminated plasma membrane complex N-glycosylated NKCC1 and transport function. Together, these results suggest that (i) NKCC1 is delivered to the plasma membrane of COS7 cells independently of its N-glycan nature, (ii) most of NKCC1 in the plasma membrane is core/hybrid-type N-glycosylated, and (iii) the minimal proportion of complex N-glycosylated NKCC1 is functionally active

Propriétés physiques des bois étudiés en 1986

Big conductance potassium (BK) channels contribute to K+ flow and electrical behavior in many cell types. Mice made null for the gene (Kcnma1) producing the BK channel (BKKO) exhibit numerous deficits in physiological functions. Breeding mice lacking a single allele of Kcnma1 (C57BL/6J background) had litter sizes of approximately eight pups. For the period of maternal care (P0– P21), pup deaths peaked at P1 with a second less severe interval of death peaking near P13. Early deaths were twice as likely during a 20-month period of building construction compared with the quiescent period after cessation of construction. Births during construction were not consistent with Mendelian predictions indicating the likelihood of a specific disadvantage induced by this environmental stressor. Later BKKO pup deaths (~P13) also were more numerous than Mendelian expectations. After weaning, weight gain was slower for BKKO mice compared with wild-type littermates: 5 g less for male BKKO mice and 4 g less for female BKKO mice. Body composition determined by quantitative magnetic resonance indicated a higher fat proportion for wild-type female mice compared with males, as well as a higher hydration ratio. Both male and female BKKO mice showed higher fat proportions than wild-type, with female BKKO mice exhibiting greater variation. Together, these results indicate that BKKO mice suffered disadvantages that lead to prenatal and perinatal death. A metabolic difference likely related to glucose handling led to the smaller body size and distinct composition for BKKO mice, suggesting a diversion of energy supplies from growth to fat storage

Phagocyte cell migration is mediated by phospholipases PLD1 and PLD2

We have investigated whether the signaling protein phospholipase D is implicated in leukocyte cell motility. Treating differentiated HL-60 cells with small interfering RNAs (siRNAs), to deplete endogenous expression of the PLD1 isoform, led to an abolishment of basal chemokinesis that could not be rescued with chemoattractants ENA-78, FMLP, and IL-8. Transient overexpression of PLD1 increased both chemokinesis and chemotaxis toward IL-8 and FMLP but not toward ENA-78. Chemokinesis was not mediated by the enzymatic activity of PLD1, but the chemotactic response was, because a lipase-inactive mutant (PLD1-K830R) negated all chemokine-induced potentiating actions and because IL-8 and FMLP increased activity in vitro. Gene expression silencing of the other mammalian isoform, PLD2, also led to cell migration arrest, whereas ENA-78 selectively increased endogenous PLD2 activity and chemotaxis of HL-60 cells overexpressing a myc-pcDNA-PLD2 construct. Thus, PLD1 is differentially activated by CXCR-1, whereas CXCR-2 (and possibly CXCR-1) mediates PLD2 activation. Finally, immunofluorescence microscopy showed that both isoforms were associated with cell polarity and directionality concomitantly with adhesion and F-actin polymerization in response to IL-8. These data represent the first demonstration of the involvement of PLD and its enzymatic activity toward chemokines in the key physiologic process of leukocyte migration