Autosomal polymorphism due to pericentric inversions in the deer mouse (peromyscus maniculatus), and some evidence of somatic segregation

Chromosoma ◽  
1966 ◽  
Vol 18 (2) ◽  
pp. 177-187 ◽  
Author(s):  
S. Ohno ◽  
C. Weiler ◽  
J. Poole ◽  
L. Christian ◽  
C. Stenius
1971 ◽  
Vol 13 (2) ◽  
pp. 277-282 ◽  
Author(s):  
Robert S. Sparkes ◽  
David T. Arakaki

Karyotype analyses of eight animals from an interbreeding colony of three subspecies of Peromyscus maniculatus (P.m. gambelli, P.m. rubidus, and P.m. sonoriensis) demonstrated a chromosomal polymorphism, probably due to pericentric inversions involving at least seven chromosomes. This polymorphism may require consideration in the cytogenetic taxonomy of these animals, and may be related to the widespread distribution of deer mice in North America and their apparent adaptability to many different environments.


2002 ◽  
Vol 83 (7) ◽  
pp. 1745-1751 ◽  
Author(s):  
Mausumi Bharadwaj ◽  
Katy Mirowsky ◽  
Chunyan Ye ◽  
Jason Botten ◽  
Barbara Masten ◽  
...  

PLoS ONE ◽  
2016 ◽  
Vol 11 (3) ◽  
pp. e0150598 ◽  
Author(s):  
Shannon W. Davis ◽  
Jessica L. Keisler

Viruses ◽  
2019 ◽  
Vol 11 (2) ◽  
pp. 183 ◽  
Author(s):  
Bryce Warner ◽  
Derek Stein ◽  
Bryan Griffin ◽  
Kevin Tierney ◽  
Anders Leung ◽  
...  

In North America, Sin Nombre virus (SNV) is the main cause of hantavirus cardiopulmonary syndrome (HCPS), a severe respiratory disease with a fatality rate of 35–40%. SNV is a zoonotic pathogen carried by deer mice (Peromyscus maniculatus), and few studies have been performed examining its transmission in deer mouse populations. Studying SNV and other hantaviruses can be difficult due to the need to propagate the virus in vivo for subsequent experiments. We show that when compared with standard intramuscular infection, the intraperitoneal infection of deer mice can be as effective in producing SNV stocks with a high viral RNA copy number, and this method of infection provides a more reproducible infection model. Furthermore, the age and sex of the infected deer mice have little effect on viral replication and shedding. We also describe a reliable model of direct experimental SNV transmission. We examined the transmission of SNV between deer mice and found that direct contact between deer mice is the main driver of SNV transmission rather than exposure to contaminated excreta/secreta, which is thought to be the main driver of transmission of the virus to humans. Furthermore, increases in heat shock responses or testosterone levels in SNV-infected deer mice do not increase the replication, shedding, or rate of transmission. Here, we have demonstrated a model for the transmission of SNV between deer mice, the natural rodent reservoir for the virus. The use of this model will have important implications for further examining SNV transmission and in developing strategies for the prevention of SNV infection in deer mouse populations.


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