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Genetics/red- brown hair but black eye brows! Am I a ginger?


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Hi, I'm fourteen and I live in Asia, in my country more than 99 percent of ppl have black hair, but my hair color is red-brown; It was complete orange until I was 11, then started to change to sth like orange-brown or red-brown, although I have all the signs of being a ginger;freckles,white skin,hazel eyes; but my eye brows are EXACTLY black! Also in my family EVERY ONE has black hair. So with this situations, I can't be sure that if I'm a ginger or not, cuz my hair color is nearly light brown, my eyebrows are black and my family have black hair. But my hair color was complete orange before till I got 12. And so my freckles are signs of being a ginger. Can you pz help me? Am I a ginger or not?! Is it possible for a ginger to have black eyebrows?!

Hi Mell! Good to hear from you!

Skin, eye, and hair color are very popular questions. Unfortunately human pigmentation is something we don't understand all that well yet genetically.

A general explanation. 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, human 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. If you look at my references at the bottom, hopefully this introduction will help those articles make more sense.

But what about skin/hair color? If we imagine a person as a factory, there is a whole department in the factory dedicated to producing the two known pigment genes, eumelanin (brownish) and pheomelanin (reddish). There are also support staff that indicate when the pigment is produced, how it is delivered, and where it goes, as well as how much the workers make. All of these factors are also controlled by DNA variations. What color we see at the end is a summation of the entire department's efforts, which could be ten or more genes. Also, the instructions on what to make can vary over time given how old the person is.
Most often people's hair darkens at maturity, then grays at seniority, but this is not a hard and fast rule.

It's actually pretty common for girl's hair color to change / darken at puberty. :) I'd say you were a ginger, but now another time-released gene has happened and your darker pigments are also coming in. It will be interesting to see what your hair does as you get older. If you have children, they will likely also be ginger when young. Ask your older relatives if they remember this happening to them. :) personally, my eyebrows were always quite dark, and I was a blonde child. Now my hair is a dark brown to match. Go figure!

There's a lot to read out there on this topic. Hopefully what I told you makes sense. Please feel free to come back if you have questions.


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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)

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