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Genetics/wildtype dogs

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Question
Dear Dr Robichaud,

I am wondering  why it is that  a dog with diverse parents -- two mongrels  or one thoroughbred and a mongrel or one thoroughbred and a very diverse mongrel-- will result in at least one puppy who appears close to the wildtype dog and looks nothing like his parents-- i.e., having almond eyes, long skinny forelegs, tawny color - often black facial mask -- (This is the wildtype dog found in India anad Africa etc.)
Why does the diversity in the parents seem to create this throwback?
I ask because I have such a puppy.  Her original parents 80 years ago were a Siberian huskie and a mastiff shepherd mix we think-- or something of the sort a "farm dog."  This puppy is the state dog of New Hampshire - the "chinook"  recognized by all official breeders organizations and considered a type of sled dog.  It is a very new breed -- 80 is young for dog breeds.
But I think that chinooks are really throwhbacks to the wild type now that I have her  -- nothing sled dog about her.  She looks just like the feral African and Indian dogs.  I love her .
My question is how did the diversity of her parents achieve this-- so different from them-- fling back? (Other breeds are achieved by mating similarity I think.)
Thank you very much for your patience in reading this long question.

Very truly yours,
Joan Pendleton

Answer
Hi Joan!

Genetics can be thought of as the 'cards' we're dealt at conception. What does this mean? When a lady makes egg cells, her body takes all her genes, shuffles them like cards, and then deals out one-half a deck to each cell. Guys do the same thing with sperm cells. When a baby is made, his and her DNA half-decks are combined to make a full deck of genes for each child. The number of cards (genes) is fixed. However, the pictures on the cards are not 'one of two colors or four suits'. Really, inheritance has many possible pictures for each card number. We call different pictures in each card position 'alleles'. The total combination of card values/alleles will affect the outward appearance of the children, who gets one allele 'picture' from each parent.  True for men and dogs.

Traits and types sometimes inherit together. Not only that, but these batches of inherited traits may be what geneticists call 'recessive', meaning that other traits can mask their presence. What you've observed with the Chinook out crosses flinging back to similar founding breeds is perfectly normal. I'm certain you've met some people who have traits dissimilar to their parents', but identical to their grandparents? It's a similar story.

If you're curious, this is why the dog breeders stipulate that an outcross Chinook must be bred back to Chinook stock four times before that line of dogs can be considered a purebred Chinook. What this does genetically is make an effort to select for the desired Chinook traits, and keep unwanted recessive traits from popping up. A similar strategy is done for scientific mouse lines, although they are back-crossed ten times instead of four. (Fortunately, it doesn't take as long to raise mice.)

Link you might find interesting:
http://en.wikipedia.org/wiki/Recessive

Please contact me if you have further questions. :)

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Trista Robichaud, PhD

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No homework questions, especially ones copied and pasted from textbooks. I will answer questions about principles or give hints, but I do not do other's homework. I'm comfortable answering basic biochemistry, chemistry, genetics, and biology questions up to and including an undergraduate level of understanding. This includes molecular biology, protein purification, and genetics. My training/inclination is primarily in structural biology, or how the shapes of things affect their function. Other interests include protein design, protein engineering, enzyme kinetics, and metabolic diseases such as cancer, atherosclerosis, and diabetes. Regrettably, I cannot diagnose any disease. I can tell you how we currently understand the basic science behind a disease state, but I cannot recommend treatment in any way. Please direct such questions to your medical professional.

Experience

I hold a PhD in Biomedical Science from the University of Massachusetts Medical School in Worcester. I specialize in Biochemistry, with a focus on protein chemistry. My thesis work involved the structure and functions of the human glucose transporter 1. (hGLUT1) Currently I am a postdoc working in peptide (mini-protein) design and enzymology at the University of Texas Health Science Center in San Antonio, Texas. I am in Bjorn Steffensen's lab, researching inhibitors of gelatinase A, a matrix metalloproteinase. I have also been answering Chemistry/Biochemistry questions on this site since summer 2010.

Organizations
2001 American Association for the Advancement of Science, 2007 American Chemical Society 2007 Protein Society 2011 UTHSCSA Women’s Faculty Association

Publications
Publications Levine KB, Robichaud TK, Hamill S, Sultzman LA, Carruthers A. Properties of the human erythrocyte glucose transport protein are determined by cellular context. Biochemistry 44(15):5606-16, 2005. (PMID 15823019) Robichaud TK, Appleyard AN, Herbert RB, Henderson PJ, Carruthers A “Determinants of ligand binding affinity and cooperativity at the GLUT1 endofacial site” Biochemistry 50(15):3137-48, 2011. (PMID 21384913) Xu X, Mikhailova M, Chen Z, Pal S, Robichaud TK, Lafer EM, Baber S, Steffensen B. “Peptide from the C-terminal domain of tissue inhibitor of matrix metalloproteinases-2 (TIMP-2) inhibits membrane activation of matrix metalloproteinase-2 (MMP-2)” Matrix Biol. 2011 Sep;30(7-8):404-12. (PMID: 21839835) Robichaud TK, Steffensen B, Fields GB. Exosite interactions impact matrix metalloproteinase collagen specificities. J Biol Chem. 2011 Oct 28;286(43):37535-42 (PMID: 21896477) Poster Abstracts: Robichaud TK, Carruthers. A Mutagenesis of the Human type 1 glucose transporter exit site: A functional study. ACS 234th Meeting, Boston MA. Division of Biological Chemistry, 2007 Robichaud TK, Bhowmick M, Tokmina-Roszyk D, Fields GB “Synthesis and Analysis of MT1-MMP Peptide Inhibitors” Biological Chemistry Division of the Protein Society Meeting, San Diego CA 2010 Robichaud TK; Tokmina-Roszyk D; Steffensen B and Fields GB “Exosite Interactions Determine Matrix Metalloproteinase Specificities” Gordon Research Conference on Matrix Metalloproteinase Biology, Bristol RI 2011

Education/Credentials
INSTITUTION AND LOCATION DEGREE (if applicable) YEAR(s) FIELD OF STUDY Oakland University, Auburn Hills MI BS 1993-1998 Biochemistry University of Massachusetts Medical School, Worcester MA PhD 2001-2008 Biochemistry & Molecular Pharmacology University of Texas Health Science Center, San Antonio TX Postdoc 2009-Present Biochemistry

Awards and Honors
1998 Honors College Graduate, Oakland University 2009 Institutional National Research Service Award, Pathobiology of Occlusive Vascular Disease T32 HL07446 2011 1st Place, Best Postdoctoral Poster, Dental Science Symposium, UTHSCSA, April 2011

Past/Present Clients
Invited Seminars: Robichaud TK, Fields GB. “Synthesis and Analysis of MTI-MMP Triple Helical Peptide Inhibitors” Pathology Research Conference, University of Texas Health Science Center San Antonio Pathology Department (June 18th, 2010) Robichaud TK & Hill, B “How To Give A Great Scientific Talk” Invited Lecture, Pathobiology of Occlusive Vascular Disease Seminars, UTHSCSA (Nov 11th 2010), Cardiology Seminar Series, Texas Research Park (Feb 21st, 2011) Robichaud TK; Tokmina-Roszyk D; Steffensen B and Fields GB “Exosite Interactions Determine Matrix Metalloproteinase Specificities” Gordon-Keenan Research Seminar “Everything You Wanted to Know About Matrix Metalloproteinases But Were Afraid to Ask” Bristol, RI (Aug 6th, 2011)

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