You are here:

Genetics/Chimera cat


QUESTION: I read that it is not possible for both dilute and non-diluted coat colors to exist on one cat. Having both would mean that the cat is a possible chimera but would need skin sample testing to confirm. If this is true, would that apply to a combination of non- dilute pitch black and a diluted orange such as "apricot" or "cream"?"

ANSWER: Hello Sam!

Usually a black cat with orange is a tortoiseshell or calico kitty, as the genes for pigmentation are on the X chromosome. When the kitty embryo is developing there is a point in the embryo when half of the X chromosomes are inactivated. Since this is random, it produces the striking fur variations of calico and tortoiseshell cats.

I did some research and the dilution gene is not on the X chromosome. (See Therefore, it's unlikely that a cat would display nondilute fur on one 'side' and dilute fur on the other. Technically, 'dilution' causes uneven distribution of color on the hair shaft.

Another uneven color distribution on the hair shaft is 'Agouti', which produces ticked (almost striped) fur. Variations of location for Agouti may alter the 'orange' side of the kitty and perhaps give the semblance of dilution. ( and

Another possibility is that the kitty in question has a mutant pheomelanin (orange) pigment such that it does not work so well, resulting in a lighter shade.

Chimerism is possible in cats; usually a chimera cat is spotted by being a male calico. Male calicos are either chimeras or have two X chromosomes in addition to the Y.

The most important thing to remember in genetics, however, is that the genome acts as instructions for a cellular corporation to produce a singular product: the cat. We have yet to figure out how all the genes interact with one another, so the possibilities are infinite. :)

---------- FOLLOW-UP ----------

QUESTION: Mutant pheomelanin pigment is something I've never heard before. Could that affect some parts of the coat an not others? the cat I'm questioning has a typical tortie shade of orange spot on the center of her head. She has one paw completely pitch black, even her nails are black. She has some orange patches are a much lighter dilute peach shade. The rest of her body is primarily ticked with a mix of straight black and either the normal orange and the diluted peach shade. Check out this page

Great page! That was a fun read.

Nope, if the pheomelanin was broken we wouldn't see deep orange.

Are you certain the lighter patches are not simply where your kitty 's Bulls-eye or mackerel tabby striping is evident? That light/dark patterning will still occur in tortie and actually is imprinted on the skin under black fur. (It's just hard to see on a black cat, though sometimes you can see 'stripe ghosts' when the cat is in direct sunlight.) You could be observing just the lighter patterned sections.

if your kitty was not a twins chimera and was dilute, she would be apricot or cream and gray/blue with no pure black.

If your kitty was a tortie with pure black that was not a chimera, she's not dilute.

If your kitty is the result of two embryos combining, some may be cream and the rest pure black. This is because one embryo may express the dilute gene while the other does not. It would also be possible for one 'side' of the chimera to be tortie while the other isn't, resulting in some striking coat patterns. :)

A genetic test may be required to know for sure.



All Answers

Answers by Expert:

Ask Experts


Trista Robichaud, PhD


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.


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.

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

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

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)

©2017 All rights reserved.