The malagarasi river does not form an absolute barrier to chimpanzee movement in Western Tanzania
Authors: Leslie A Knapp
Patricia A Crystal
Fiona A Stewart
Yingying Li
Alex K Piel
Lilian Pintea
Dorothy E Loy
Miguel A Ramirez
Gerald H Learn
Beatrice H Hahn
Paul M Sharp
Journal: PLoS ONE (2013)
Discipline: Multidisciplinary
Keywords: Malagarasi River; chimpanzee movements; gene flow; population connectivity; pathogen transmission
Affiliations: Department of Anthropology, University of California San Diego, San Diego, California, United States of America. 

Abstract:  The Malagarasi River has long been thought to be a barrier to chimpanzee movements in western Tanzania. This potential geographic boundary could affect chimpanzee ranging behavior, population connectivity and pathogen transmission, and thus has implications for conservation strategies and government policy. Indeed, based on mitochondrial DNA sequence comparisons it was recently argued that chimpanzees from communities to the north and to the south of the Malagarasi are surprisingly distantly related, suggesting that the river prevents gene flow. To investigate this, we conducted a survey along the Malagarasi River. We found a ford comprised of rocks that researchers could cross on foot. On a trail leading to this ford, we collected 13 fresh fecal samples containing chimpanzee DNA, two of which tested positive for SIVcpz. We also found chimpanzee feces within the riverbed. Taken together, this evidence suggests that the Malagarasi River is not an absolute barrier to chimpanzee movements and communities from the areas to the north and south should be considered a single population. These results have important consequences for our understanding of gene flow, disease dynamics and conservation management. 

Retracted: No

PubPeer comments:
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 Figure 1:  Modulation on insulin sensitivity by GRK2. Immortalized murine white adipocytes and C2C12 myocytes were transiently transfected with empty vector (control, C), pcDNA3-GRK2-neo (+), the catalytically inactive pcDNA3-GRK2u2013K220R (K), or shGRK2-RNAi (u2212) to upregulate or knock-down GRK2 expression, respectively. **A**: Lysates were analyzed by Western blot with the corresponding antibodies against GRK2 and u03b2-actin. ... **(D)** myocytic cell lines were serum-starved overnight and then incubated in the absence or presence of 10 nmol l insulin (Ins) for 10 min.  The Myocyte slices of 1A are clearly re-used from 1D, but the experiments appear to be different; there is no talk of serum-starvation or + - insulin for 1A. Am I missing something? The figure legend refers to Supplementary Figures for full blots, where  Blots shown in S3(A) correspond to experiments performed for Figure 1A; S3(B) for Figure 1C , but this does not help us for Fig 1D, while S3(A) only shows the adipocyte blot. , 
 Fig 1:  ... For examples of full-length blots, see supplementary Fig. S3, available in an online appendix. ... For examples of full-length blots, see supplementary Fig. S3. Where S3(B) corresponds to the results of Figure 1C, according to the Supplement.  These  full-length blot examples only appear to show the P-AKT and P-ERK 1 2 bands. One of the examples seems to have provided the P-ERK 1 2 slice shown in Fig 1C, but other slices appear have originated in different blots. Am I missing something? , 
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